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empreinte. 

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symbola  V  signifie  "FIN". 


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method: 


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Lorsque  le  document  est  trop  grand  pour  itre 
reproduit  en  un  seul  clichi.  11  est  film*  A  partir 
de  Tangle  supirieur  gauche,  de  gauche  A  droite, 
et  de  haut  en  bes.  en  prenant  le  nombre 
d'images  nicessaire.  Les  diagrammes  suivants 
illustrent  la  mithode. 


1 

2 

3 

1  2  3 

4  5  6 


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PLATE  I. 


STBrtTIKFJ^  <IK  THK   NoKMAL   KiDNKY. 

1,  ("apsuln;  2,  convoluted  tubulo:  a,  outor  layer  of  the  capsiilo;  4,  intervening  spare: 
5,  rctlecti'il  (Kirtion  of  the  fapsuU>;  f>.  ilistal  eonvohileil  tvilmle;  7,  irreguhir  iKjrtion  of 
distal  eonvohiled  tubule;  S,  eml  iiortiim  of  distal  convoluteil  tuhule;  >»,  rollecl injr 
tuhule;  10,  aseendini;  loop  of  Ilenle:  II,  arteria  reeta:  12,  vena  recta;  i:{,  liK)p  of 
llenle;  14,  pyramid;  l,"),  papilla;  Ui,  papillary  vascular  plexus:  17,  main  collecting 
tubule;  IS,  calix;  1!),  boundary  zone;  20,  larger  brancli  of  renal  vein;  21.  larger  brancli 
of  renal  artery;  22,  ilescemling  limp  of  Henle;  2:i,  interlobular  vein,  collecting  from  the 
stellate  (dexus;  24,  narrow  portion  of  aso<'nding  loop  of  Henle;  25,  interlobular  vein; 
■-'(■>,  interlobular  artery;  27,  gloiiienilar  capillary  network;  28,  stellate  plexus  of  caj)il- 
laries;  2!l,  efTerenI  vessel;  30,  alTerent  vessel. 


THE    ANATOMIC 
HISTOLOGICAL    PROCESSES 


OF 


BRIGHT'S  DISEASE 

AM)  THF.IR   RKLATION    lO    THE  Fl'NC'ION  \l,  CHANGKS 


LECnRKS    DKLIVKRtD    IN    THK 

RISSKI.I,    SA(iK    INSirri   TK    OF    HATH()LO(]Y 

CllY    HOSPITAL,    NKW    YORK 
Oi  HIM.    iH»    WiNim   ti*    I90y 


BY 

HORST  OERTEL 

l'lll»>   Ion    lit      |H»     KI^^H.|.    s»i,,     IWIITITK    "►     KA  IHiil  iir.V,     \».»     Vi)«« 


//, /,  LS  r  R  J  IF  I) 


PMII.ADKI.I-IIIA    AM)    t.DSDON 

W.    B.   SAUNDERS    COMPANY 

1910 


<  iii'vidi.iii ,  I'.iKt.  in   \\  .  M,  Smmikio  (iimi'vs^ 


rKIVTKl)     IN     AMKHII    V 


KDWAUIXi.  .lAM.WAV 


M'HIK.M    IMK  ^<  IKSIIHl     I'll  \.    I  I.  f;  1  It    MKllll  INK    I  \     ^\IKCI•^ 

"'H^.^.  \  m:\\\  nuiii.  wdwiiiimk  \ikiimiiis.   wikik 


I  IIMI' 


l>.ll«t.\l»  KWK,    \l     \l.l.    lIMKf 


III  KN    KWMI'I.I.    Mil.     Wll     ISKI-lllt. 

n<>\.   i\  i.\si  iM,  i.KMiii  iif: 


PREFACE 


Tmksk  loclun-s  wMc  «l«'livcn'(l  at  tin-  mjiu'st  (»f  tln'  Ui-sulciit 
Staff  (tf  the  New  York  City  Hospital  in  tlir  HtKsrll  Saji*'  In- 
stitute of  Patlii»|o;ry.  during  the  wintrr  scimstcr  MMIN  to  11MM> 
Iw'forc  an  audience  of  recent  v:ra(luat<'s  and  some  advained  nndcr- 
^T-'duates  in  medicine.  My  liearers  wished  to  olttain  in  syste- 
matic and  coimected  form  tli«' almost  daily  ex'iM'rience  in  hospital 
and  |)atholo<ri<-al  institute.  Tliey  wanted  j.rimarily  to  intelli- 
j:('ntly  understand  what  they  .saw  at  tlie  In-dside  and  at  the 
autopsy  tal)le. 

The  lectures  deal,  therefore,  with  the  morphology  of  nephritis, 
and  in  a  somewhat  ditfj-rent  form  from  the  u.Mial  manner.  Kvery- 
where  I  have  endeavored  to  particularly  emphn.size  relation.s 
and  to  reconstruct  the  whole  as  a  miit  of  interwoven  proce.sKes, 
rather  tlian  a  mere  .statement  of  facts.  As  this  method  of  treat- 
ment may  not  he  unwelcom*.  to  a  wider  medical  public  and,  as 
far  as  I  know,  does  not  exi.st  in  Knjr|ish  literature,  I  now  pub- 
lish them  practically  in  the  form  of  the  steno^jraphic  reiM)rt, 
except  for  some  additions  and  explanatory-  notes.  This  accounts 
for  an  unevemiess  of  treatment  and  some  local  colorinjr  in  the 
presented  material. 

I  may,  perhaps,  l)e  pardoned  if  I  tpialify  here  my  .stand  in 
teachin-i  medicine  and  particularly  patholojry  in  some  detail. 
The  average  .American  medical  student  ot  the  present  day  is 
taujrht  in  his  colle<;e  a  larjte  variety  of  medical  subjects,  but  in  a 

V 


I'HKK'«'K 


niaiiiicr  which,  acconiiiiir  t'>  my  cxiMM-iciicc,  is  not  apt  to  develop 
ill  him  a  plastic,  hviii<;  and  ficxihic  conception  in  any  sul)ject,  in 
other  words,  no  independent  thoujiht.  Force<l  hy  ;•  rijiid,  pre- 
scrihed  schechile,  whicli  I(>aves  him  no  academic  freedom,  in- 
divicUial  responsiliility  and  time  for  thoroiijihness,  he  memorizes, 
mostly  from  text  l»ooi<s,  lectures  and  r(>citations.  and  discon- 
nected demonstrations  and  clinics  many  statements  and  some 
facts.  His  coticeptions  are  those  of  a  certain  text-hook,  of  a 
certain  pii-ic.  or,  similarly,  of  notes  of  a  certain  instriictor.  They 
are,  if  the  term  is  permissible,  fossilized  and  immovable.  The 
ability  derived  from  personal,  well  directed  experience  under  an 
in.stnictor,  the  ability  to  form  plastic  pictures  of  occurrences 
which  enable  one  to  comi)ine  visual  and  live,  true  itleas  of  patho- 
lojiical  proce.sses  without  becomin^^  unreliable  and  ,*.iantastic. 
are  foreiun  to  most  of  our  |)resent  medical  .ireneration.  Thus, 
our  present  methods  of  teaching  resemble  the  dead  inflexible 
formalism  of  the  scholastic  period  tau>>;ht  in  the  F.ni'.pean  uni- 
versities durinji  the  middle  aj^es. 

The  medical  irraduate  of  to-day  enters  a  hospital,  faces  life 
and  meets  the  keene.st  disappointment.  His  hard  and  fast 
text-book  lines  and  schoolboy  classifications,  memorized  care- 
fully for  recitation  and  writteji  examinations,  are  broken  and 
shattered.  Hut  wor.se,  havinii  no  other  foundation,  no  critic-il 
judf-nient  of  relative  values,  which  is  derived  from  historical 
knowl(>(lii('  of  a  science,  he  is  unable  to  utilize  his  new  experi- 
ence. He  holds  new  parts  of  a  chain,  but  cannot  unite  them, 
nnich  less  link  them  to  the  old.  It  takes  a  stron<>-  mind,  much 
stron^icr  than  the  average  medical  jiraduate  has,  to  evolve 
successfully  out  of  thes(>  complicated  circumstances.  The  others 
are  si?nply  c(,ntent  to  airain  memorize  actual  experience  in  the 
Hospital,  and  apply  it  as  well  as  they  can.  They  remain  un- 
cultured. 


PKEFACE 


Vll 


Horpiii  lip.s  a  dpfifipiicv  of  our  system  of  instruction.  "  Die 
Welt  (les  Sehenden,"  I  liave  heard  Winu't  impressively  say  in 
one  of  his  lectures,  when  I  was  a  student  in  lieipzijr,  "  ist  die  der 
(Jesichtsvorstellun^ren."  This  view  of  the  jrreat  psycholofjist 
is  amply  followed  in  all  l';uro{)ean  universities.  .Medical  teach- 
injr  is  prijnarily  directed  toward  developing;  the  power  of  ol)- 
jective  oh.servation  and  a  scientific  method  of  thinkinj?.  In- 
.struction  is  <-iven  not  outside  of  the  hospital,  but  in  the  hos- 
pitals and  iti  the  autop.sy  rooms  where  things  can  he  seen,  with 
much  personal  freedom  in  work  and  study.  .Xothinji  is  more 
important  in  the  education  of  a  physician  than  the  development 
of  clear  visual,  anatomical  ideas  of  diseased  processes  and  ability 
to  con.struct  their  po.ssii)!e  relations.  The  importance  of  this 
"anatomical  idea"  in  the  education  of  the  i)hysician  was  con- 
stantly empha.sized  l>y  Charcot  and  X'irchow. 

It  is  to  he  rej-retted,  therefore,  that  unfortunate  circum- 
stances still  make  it  impo.s.sil)le  to  conduct  most  of  our  lar<>e 
hospitals  as  academic  institutions. 

Hut  I  also  view  with  some  fear  for  our  future  in  medical  educa- 
tion the  present  tendency  in  some  of  our  medical  collejies  to 
introduce  s|)ecialized  branches  of  patholof-y,  medicine  and 
surj-ery  into  their  underjrraduate  courses  at  the  expense  of  the 
morpholo-ical  discipline,  instead  of  a  -reater  effort  to  properly 
develop  the  opportunities  of  the  latter  in  its  relation  to  clinical 
medicine.  I  would  not  deny  their  value.  Indeed  experimental 
patholof-y,  medicine  and  surjiery  are  very  neces.sary  supplements 
or  better  complements  of  morphology  for  the  elucidation  of 
sjK'cial  proi,lems  and  in  the  hands  of  experienced  patholo-ical 
anatomists;  they  are  suited  particularly  for  advanced  students. 
But  thex-  can  never  replace  that  knowledf^o  which  is  obtained 
from  tlie  study  of  a  disea.se.  The  latter  is  an  experiment  of 
nature  which  develops  out  of  ever-varyinji,  complicated,  external 


Vlll 


PHKKACK 


:iii(l  ititcriiiil  coiKlitioiis  wliich  we  ciimiot  exactly  artificially 
duplicate  in  causes,  nuniher,  time  and  expressions.* 

NO  less  a  inilliaiit  experimental  investiirator  and  leader  in 
experim(>ntal  pat  hole tiiy  than  Colinlieim  significantly  delivered 
his  own  inauiiural  address  in  assuminu;  the  chair  in  jieneral 
patholojiv  in  the  I'niversity  of  I^>ij)zi.!i.  "  I'eher  die  Auf<ial)en 
der  patholofiischeii  Anatomic." 

It  is.  indeed,  a  serious  prol)lem  which  confronts  today,  not 
only  the  i-cneral  medical  education  of  our  younjier  <reneration  of 
students,  hut  that  of  the  developinji  pathologists,  .\lready  a 
lack  of  thorouiih  patholoiiic  anatomical  knowlediic  experience 
and  depth  of  thouiiht  liecomcs  noticeahle  in  nuich  of  the  recent 
patholoiiical  literature  on  the  i)art  of  many  of  those  who  have 
followed  a  one-si(l(>(l  and  more  spectacular  spi'cialization  in 
patholoiiical  research  without  soimd  anatomical  foundation. 
Those  who  douht  my  words  should  read  the  warnin<r  of  Orth  in 
that  matter.  "  Zur  B<>zeichnun,u-  der  IWisartijien  epithelialen 
Xeuhilduniicn."  Zentrallilatt  f.  allii.  I'ath.  u.  path,  anat.,  11, 
MXIS.  and  v.  Ilansemann  in  Zeitschrift  f.  Krel)sforschun<>\  Vol. 
\II.   1  !)(»<». 

.\  spirit  of  anatomical  renaissance,  therefore,  permeates 
these  lectiu-es.  Hut  I  h.ive  .ilso  endeavored  to  emphasize  what 
Cohnheim  in  his  inaujrural  address  s;iid  of  patholojiical  anatomy 
as  contrasted  with  normal  anatomy:  "Die  p;itholo<:ische  Ana- 
tomic ist  ,u;u-  nicht  eine  deskriptive  W'isen.schaft  in  dem  Sinne 
wie  es  die  normale  ist ."  Pat  holouical  anatomy  is  an  explanatory 
discipline.  Its  (>ducational  v.ilue  is  therefore  twofold:  It  pre- 
sents the  visual  picture  of  a  process  and  it  discloses  the  irenesis 

*  ( 'i)in|>Mic  llic  idni'liuliiin  remarks  of  Marcli;iiiil  in  llic  ilcscriptiim  of  the  nrw 
pallidliUjiial  inslinitc  at  I.i-ipzitf  in  llic  IVst.sclirift  fur  the  .")0()tli  aniiivrrsrir.v  of  tlic 
riii\crf.ily  III  Austria  a  very  ilcsiralilc  si-paralioii  of  patliolouy  into  two  cliairs,  patlio- 
ioiiii-al  aiiatoiiiy  ami  cxpcriiiiciilal  pallio!o(jy.  li.as  alrraily  taken  plaee;  in  (ierinany  the 
latter  is  now  taimlit  by  eliniciaiis.  'I'lie  siliiation  is  very  similar  to  the  state  of  pliy-iolo(jv 
anil  anatomy  lifty  vears  a(jo. 


PHEFACE 


IX 


of  the  process,  at  least,  prepares  the  proper  way  for  its  uiider- 
staiuUnji.  These  iM)iiits  I  had  constantly  before  my  eyes  in 
the  delivery  of  these  lectures. 

Some  may  find,  perhaps,  a  more  extensive  review  of  ele- 
mentarv  and  jreneral  patholoj-ical  questions  than  may  seem 
warranted  to  them  hy  the  nature  of  the  subject  in  a  jiraduate 
course,  .\fter  deliberation,  I  have  (-)ncluded,  however,  not  to 
eliminate  them  in  the  publication  of  these  lectures,  for  the  activ- 
Uy  of  invest ijiators  has  been  so  productive  that  such  reviews 
mi«iht  possibly  be  welcome  to  tho.se  who  have  been  unable  to 
completely  follow  the.se  subjects.  Some  of  them  have  had 
important  contributions  since  these  lectures  were  ready  for 
publication.  Particularly  in  the  doctrine  of  fat  dejieneration 
and  fat  infiltration,  the  views  still  underj-o  a  kaleidoscopic 
cliaii.iic 

Many  of  the  ideas  expres.sed  in  the  following;  pajres  are  ba.sed 
on  data  collected  by  me  and  former  and  present  assistants  dur- 
inji  a  period  of  six  years  at  the  City  Ho.spital.  My  f-reate.st 
indebtedness  is  to  Dr.  I.indsay  .Milne,  who  has  .sacrificed  nuich 
of  his  own  time  and  thouj-ht,  and  to  whom  I  owe  the  selec- 
tion of  typicjil  pictures  for  the  acccmpanyinji  plates.  They 
wer(>  execut(>d  by  Mr.  Martin,  the  artist  of  the  Hu.ssell  Sajje  In- 
stitute, '{"he  -renerosity  of  the  Trustees  of  the  Hu.s.sell  Sa<re 
Institute  made  th(>  publication  possible.  To  the  publishers  I 
owe  very  hearty  cooperation  and  valuable  sufr-iestions. 

I  may  fittinjrly  introduce  these  lectures  after  the  manner  of 
Morfrajrni  in  his  j-reat  "  De  sedibus  et  cau.sis  morlwrum  per 
anatomem  inda,iiatis:"  ("ra.s.sus  in  Cicero,  '  De  oratore,"  II, 
0.  2'),  quotes  Lucilius  as  follows:  "  C.  Lucilius,  homo  et  doetu.s 
et  |XM-urbamis  dicere  .solebat  najiw  .sr  ah  itulortissitnis  ncque  a 
(loctittsiniis  k(fi  vcllc,  quod  nlteri  nihil  intclhqercnt,  alkri  plus 
/o//rt.s.sr  quniu  i/isc."     •'  C.  Lucilius,  a  lejirned  and  ver>-  polished 


X  PKEFACE 

man  was  in  tho  habit  of  sayinji  that  he  did  nol  irish  to  hr  rend 
cither  bjf  the  vcrtf  learned  nor  hi/  the  very  iinediieated:  for  the  latter 
would  not  nn<terstand  him,  while  the  former  mii/ht  ]>ossibly  knoir 
more  than  he  himself  did." 

IIoHST  Okutki,. 

HvKsKi.i.  Sauk   Instititk  ok  I'ATiiDi.iiiiV.  Cirv   IIiisi'itai,, 
Nkw   Vokk  City,  Vd/v  «((«)•,  IHIo. 


CONTENTS 


FIRST  LECTURE  ,.„,y, 

UlSTOKK  Al,  InTKODICTION  AND  C'lASSIKICATION 1 

SECOND  LECTURE 
Tin;  Stui fTiiiK  of  thk  Normal  Kidney  and  thk  Diffehknt  Views 
OS  Its  P\ncti(>ns  in  Tiieik  Relation  to  the   Patiiol()(;i(al 
\'ahiatio.vs 27 

THIRD  LECTURE 
The  De«!Eneuati\  e  and  Exioative  Featikes  of  Nephhitis  4.") 

FOURTH  LECTURE 
The  Rksilts  and  Tekminations  of  Degenerative  and  Exidative 

NeI'IIHITIS.       i'ltODlCTIVE  CllAN(iES  IN  THE  KiDNEY IK) 

FIFTH  LECTURE 

FUODK  TIVE  XEl'ilHITIS.       CllANOES  IN  OtHEK  ViscEHA.       (EdEMA 1()1 

Notes  and  References .7jjj 

AlM'ENDIX .,.  , 

Classification  of  Nephritis 014 

Non-inrtaniniatory  Lesions  of  the  Kidney,  Oecasionally,  l)ut  Wrongly, 

Grouped  as  Nepliritis '^14 

Index  of  Names ,-,,- 

iu 

Index  ok  Sl'h.iectis 291 


THE  ANATOMIC 

HISTOLOGICAL  PROCESSES  OF 

BRIGHT'S  DISEASE 


FIRST  LIXTUHE* 

HlSTOHICAL   I.NTKODrCTIOX   AND   ClassificATIOX 

(lenthmoi:  , 

It  is  with  -reat  pleasure  that  I  have  followed  ^•our  invitation 
to  speak  to  you  about  the  diseases  of  the  kidnev  ordinarily 
grouped  as  Brijrht's  disease.  But  I  appreciate,  and'l  think  vou 
probably  will  before  I  finish  these  lectures,  the  ^^eat  difficulties 
which  prese,it  themselves  in  a  study  of  renal  lesions,  and  more 
particularly  ui  that  -roup  which  we  intend  to  discuss. 

The  diseases  of  the  kidney  differ  in  a  peculiar  wav  from  the 
diseases  of  other  or-ans.   Three  points  enter  into  this. 

First,  there  exists  an  exceptional,  intimate  correlation  of  the 
diseases  of  the  kidney  with  concomitant  or  associated  conditions 
which  we  cannot  dismiss  from  our  consideration  as  we  do  in  the 
study  of  other  orjians.  To  illustrate  this  concretelv  I  mav  sav 
that  one  can  investij^ate  the  inflammations  of  the  lu.iji,  of  the 
heart  of  the  liver,  or  of  the  spleen,  more  or  less  independently 
of  other  organs.  We  can  abstract  them  from  the  rest  of  the 
^ody,  so  to  speak,  and  observe  them  independentlv.  This  is 
I'ardly  po.ssible,  however,  in  the  diseases  of  the  kidnev,  more 
especially  in  Brij^ht's  disease.     I  need  only  to  remind  you  that 

*Deliverp<l  on  .January  14,  liKH). 


nmciIT  S    DISKASK 


the  (|U('sti<)ns  t»f  liypcrtrophy  of  the  hcMit.  of  (I'dciiiii.  of  circula- 
tory (lislurlianccs,  of  cliaiijics  in  the  hlctod-vessds.  of  all>uiiiiii- 
uria,  etc..  arc  so  iiitiiualcly  coimcctcd  with  tlic  cliaiiKcs  in  the 
kithicys  that  it  hccoincs  (>vi(lcnt  at  once  that  licrcin  iics  a  con- 
sidcralily  coinplicatinii  factor. 

Socondly.  tiicrc  exists  irreat  difhculty,  and  at  the  same  time  a 
much  greater  necessity  here  than  in  ahnost  any  other  orjjan.  in 
estahlishinfi  a  pntper  relationship  Ix'tween  structural  and  func- 
tional changes.  \U\t  not  only  are  we  almost  entirely  ijinorant, 
or  at  least  uncertain,  of  many  of  the  physiolojiical  conditions  of 
the  secretion  and  of  the  part  played  therein  by  the  various  com- 
ponents of  the  kidney,  l)Ut  in  the  patholoj^ical  variations  we  are 
constantly  confronted  l)y  obstacles  which  consequently  are  hard 
or  e\en  impossible  to  overcome. 

Finally,  a  third  factor  which  conflicts,  and  a  rather  personal 
one,  is  the  multitude  of  views  held  with  rejrard  to  the  normal  and 
patholojiical  functions  and  the  anatcmiical  and  histolofjical 
chanjics  in  the  kidney,  which,  on  account  of  their  number  and 
of  the  peculiar  subjective  tendency  here  displayed,  make  it 
almost  impossible  to  present  them  .satisfactorily  and  entirely. 

It  is  by  reason  of  these  conflict  inn-  opinions  that  the  presenta- 
tion of  the  subject  is  diflicult,  and  it  will  undoul)tedly  plainly 
appear  when  I  review  for  you  in  a  necessarily  short  and  circum- 
scribed way  the  evolution  of  tiie  various  conceptions  of  the 
character  of  Brii-ht's  disea.sc.  To  a  ^reat  extent  this  is  respon- 
sible for  the  uncertainty  which  exists  even  to-day. 

This  leads  me  to  (pialify  the  necessity  of  such  a  historical 
review.  It  is,  no  doubt,  interestinj;;  and  instructive  to  follow 
the  historical  development  of  the  various  views  held  al)out  any 
disea.se;  but  I  consider  it  imperative  in  the  diseases  of  the  kidney, 
because  it  is  im{)ossil)le  to  have  an  appreciation  of  the  relative 
value  of  the  present  ideas,  unles.s  we  are  fully  acquainted  with 


HISTOHICAI,   INTHODl CTION    AM)   (I.ASSincATIO.V  3 

tho  ori«i„  „f  thos..  ideas  a,.,l  tho  (lrvelopmo„t,s  thr.„.jih  which 
they  have  passed. 

It  apiM'ars  (hat  there  are  es«.,.tially  three  interwoven  dis- 
I""«'<1  IxMiits.  and.  as  you  will  see.  fundamental  ones.  Th.-  first 
IS.  What  u.Han,nmtions  of  the  kidney  are  to  be  in<-luded  under 
♦'"'  J»"'din^r  of  Brijihfs  diseas«.?  The  seeond.  What  are  th.. 
••hara<-t(.ristic  features  (,f  this  inflammation?  Ihe  third  Are 
there  any  non-inflaumuitory  proee.s.ses  which  form  es.s^ntial 
parts  of  this  disease? 

Of  them.  I  consider  the  second  the  most  imixirtant.  It  is 
oa.sy  for  you  to  appreciate  that  whatever  conception  mav  l,e 
held  of  an  inflammaton-  con.lition  of  the  kidney  is  necesslirilv 
dependent  ur,on  the  view  o,>e  has  of  inflammation  in  ^^eneraj- 
and  the  various  views  which  have  \>een  advanced  from  time  to 
Ume  center  around  the  evolution  of  this  ^eneral  pathological 
conception. 

One  nristake.  too  frequently  made  as  the  result  of  histolo.dcal 
stu.l.es.  IS  to  re,.ird  pathological  pro,.e.s.ses  as  stationar^;  in- 
flex.hle.  of  .reat  m.iformity  in  appearan.-e.  or  at  least  froin«  on 
with  mathematical  precision  in  temporary  arranjjement.     One 
oujrht  to  appre,.i.,e  from  the  start  that,  as  the  name  implies 
i.it  u,loo;H-d  pro..esses  are  processes;   that  is.  foivver  .-hantin. 
H..stolo,.cal!y  weol,.servesta,esof  a  process,  but  we  cannot  ime^ 
pret  them  m  the  sense  of  a  simple  introduction  of  certain  abnor- 
"•ahties  „,to  an  oroan.  where  they  lie  more  or  less  like  foreign 
-hes       .Neces.sarily.  they  c-ontinually  vary,  constantly  influ- 
ced  by  conditions  which  a.ain   depend  upon  a  lar,e  number 
of  outside  factors  and  an  equally  lar^e  numlx^r  of  ever-chansin. 
•ndivKlual  reactions  on  the  part  of   the  organism.      Stricth- 
«peak.n,.  one  mi.ht  say  that  there  are  as  many  di.seases  as  thei. 
are  disea.sed  individuals.     While  this  is  to  be  taken  into  con 
SKleration  m  the  study  of  any  disease,  it  can  much  less  be  dt 


4  HHKJIIT  S    niSKASK 

n'.i;:inl('(l  iti  nephritis.  Diseases  must  Im'  >rr<)U|H'(l,  therefore,  with 
a  tliornii<;li  appreciation  of  tliese  |H)ssil)le  variations,  and  the 
strict(>r  and  more  circumscrilx'd  a  chissifieation,  the  more  faulty 
it  will  always  he.  For  a  definition,  to  Ik-  exact  and  <'xhaustive, 
must  consi.st  in  a  rejM'tition  of  all  component  parts  of  a  sub- 
stance or  a  process.  These  it  sets  out  to  systematize.  Thus, 
as  Taine  lias  put  it.  '•un  systeme  est  une explication  de  I'ensem- 
hle  et  indicjue  ime  oeuvre  faite."  l)isea.s«'s  live,  however,  con- 
stantly chanjie,  and  develoj).  Influenced  l>y  iiuuimerahle  outside 
and  in.side  conditions,  they  defy  strict  codification  in  nuich  the 
same  mamier  that  any  form  of  life  does. 

C'.uided  l)y  such  considerations.  I  shall  not  follow  the  plan 
frecjuently  employed  hy  lecturers  in  a  too  dogmatic  and  coniplete 
pre.sentation  of  the  sul)ject.  It  will  Ik'  my  endeavor  to  pmsent 
ess<>ntially  the  certain  anatomical  and  histolojiical  kaowled<i;e 
which  has  jiradually  accinnulated  in  the  course  of  time,  and 
which  constitutes  the  fundament  of  the  whole  structure.  I  .shall 
treat  these  changes  in  their  fieiieral  genesis  and  relation  to  each 
other  and  to  the  associated  functional  di.stvirhances.  Thus,  al- 
though incomplete,  it  may  serve  you  better  for  future  thought 
and  experience  than  a  recital  of  many  unconnected  facts  and 
uleas. 

Diseases  of  the  kidney  have  been  known  for  a  very  lon<>;  time; 
even  the  Hii)le  mentions  as  imi)ortant  "to  test  a  man's  heart  and 
kidneys,"  which  nniy  indicate  a  possible  knowledjie  of  the  rela- 
tion.ship  between  heart  and  kidneys;  but  reliable  data  do  not 
appear  vmtil  more  thorough  knowledjie,  gained  by  autopsies  of 
human  l)einj:s,  drew  attention  to  certain  anatomical  chan<>;es 
which  the  kidney  may  under-io.  -lltius.  between  ;i()()-4()(»  \.  1).. 
came  to  the  conclusion  that  certain  cases  of  (edema  and  ana- 
sarca were  associated  with  hardened  kidneys.  This  knowledjje 
was  extended  on  the  clinical  side  by  an  equally  fiood  observer, 


HISTOHICAI,    INTHODrcTloN    AM)   (I.ASSIKICATION 


Avimiiiii,  !il»<iut  UMM).  who  found  that  in  a  ('citaiii  nunilKT  of 
tlicsc  cases  the  urine  was  thin,  watery  and  increased  in  (juan- 
tity.'  lint  it  was  more  especially  Mor-ianni,-' dininj!;  the  hitter 
half  of  the  eijiliteenlh  century,  whom  we  proiK-rly  re^rard  as  the 
founder  of  patliolojiieal  anatomy,  who  descrilx'd  with  fjreat  care, 
clinic.illy  and  anatomically,  cases  of  jjnnnilar,  contracted  kid- 
neys, associated  with  dro[)sy.  In  certain  other  ol)s<>rvation8 
which  he  made  in  order  to  determine  the  caus<>  of  dropsies  ho 
fouiKl  healthy  kidneys  hut  distinctly  diseased  livers.  Dropsies, 
which  were  then  regarded  as  morbid  entities,  were  therefore  clas- 
sified as  with  and  without  kidney  disease.  A  fireat  step  toward 
better  knowledge  of  the  diseases  of  the  kidney  was  made  by  ("o- 
tu-ino  in  1770,'  who  demonstrated  for  the  first  time  the  occur- 
rence of  serum-albumin  in  the  urine  of  dropsical  patients.  He 
brouudit  that  fact  into  proper  relation  with  ease.s  of  u'dema  and 
anasarca.  i'Ut  erroneously  held  that  it  represented  an  efTort  on 
the  part  of  tlie  orjranism  to  <;et  rid  of  the  (inlcMiatous  fluid. 

Cruikshank'  ehiborated  Cotufino's  fin  ,  and  found  that 

certain  cases  of  (wlema  showed  no  albumin  i  the  urine;  finally 
Wells'  demonstrated  the  presence  of  blood  and  albumin  in  the 
urine  of  scarlet  fever.  (Iradually,  then,  positive  anatomical  and 
clinical  evidence  accumulated,  which  pointed  more  or  less  closely 
to  the  connection  of  dropsy,  all)umin  in  the  urine,  and  kidney  dis- 
ease. Early  in  the  last  centur>'  the  examination  of  urine  had 
lieen  well  elaborated,  particularly  by  Brande  and  Scudamore,* 
who  already  knew  that  idbuminous  urine  contained  less  urea 
than  tlid  normal  urine. 

Brifiht's  work  was  ushered  in  by  that  preliminarv  knowledjie. 
Like  his  predecessors,  he  commenced  his  observations  with  an 
investijiation  into  the  causes  of  dropsy,  and  it  was  his  purpose  to 
determine  the  underlying  anatomical  condition.  He  collected 
and  frrouped,  ver>'  excellently  indeed,  a  certain  number  of  cases 


m  "I 


i  >1 


0 


ilKKillT  s    DISK  \^K 


(if  u'llriiia  :issii«-i:it(>(l  with  chaiiucs  in  the  kiiliicv,  mixI  in  a  similar 
fashion  certain  ras»'s  of  ascites,  anasarca,  or  tnlcina  with 
diseases  of  the  liver.  .mikI  it  is  mainly  lki>:hf's  credit  to  have 
pointed  ont  more  clearly  than  an>  one  hefore  him  that  certain 
easi's  of  dropsy  are  constantly  associated  with  cerlidn  changes 
in  the  kidneys,  and  others  (Mpially  w'lh  certain  diseases  of  the 
liver.  Thes<'  fir>-t  ol>s«'rvations  apjM'ared  in  IS27  -  a  classical 
pul>lication  illustrating:  the;ire:it  value  of  thorou;:h.  painstaking:, 
ohjective  observations  and  deductions  therefrom."  It  may  Im' 
said  that  almost  everythin;:  which  Hrijrht  advanced,  as  far  as 
pure  oliservation  j:o<'s.  has  stood  the  test  of  time  until  to-day. 
The  clinical  pictures  which  he  presented,  particularly  later,  in 
the  first  vohnne  of  the  (iuy's  Hospital  report  on  chronic  renal 
dise.'ise.  have  never  Ix'en  l»ett<'r  drawn  hy  any  later  author,  and 
to-day  we  have  no  lietter  description  than  that  he  jiave  us." 
Kven  on  the  anatomical  side  his  ol)servations  stand  to  a  jrreat 
extent  to-day.  He  properly  correlated  the  hypertrophy  of  the 
left  ventricle  of  the  heart  with  .some  diseases  of  the  kidney,  and 
he  advanced  the  same  views  with  rejrard  to  this  relation  which  are 
held  to-day.  (  Particular  attention  oujiht  to  he  paid  to  the  exe- 
cution of  the  plates  accompanying:  his  first  report  of  me<lical 
cases  in  1S27.  and  printed  in  London,  showini:  the  excellent 
workmanship  of  that  time.' 

Hriiiht  did  not,  of  course,  finish  his  work  with  this  orijrinal 
account,  luit  sul)se(juently,  in  the  (iuy's  Hospital  I{e|)orts.  he 
pul>lish(>d  a  number  of  very  important  observations,  extendinii 
his  oriiiinal  views  on  the  subject.  He  divi(h'd  the  disease  into 
three  <rroups: 

"  In  the  first  the  kidney  is  apparently  in  a  .stable  of  ilefjenera- 
tit)n.  ctiusinj:  this  orjian  to  be  les.s  firm,  yellow,  mottled.  This 
may  lead  to  an  alteration  characterized  by  a  tulierous  appearance 
of  the  surface. 


IIISTOHH  Al.    INTKOI)    rTION    AND    CI.ASSIKlCATlnN  7 

"  In  the  wmoikI,  tlu'  ki('iH>y  is  traiisforiiHMl  into  a  jjraiiulatiKl 
H'xtun'.  as  if  tine  fjraiiis  of  ^'••u^l  had  Ihm'II  spriuklod  over  it.  ami 
wMiu'titncs  innmiH'ral.l.'  s|MM-ks,  of  no  clrfinito  form,  an'  eciually 
sln-wn  over  llx'  surface.  I-itrr,  tlu"  kidiu'V  assunu-H  a  tuln'roiw 
;i|)|M'araiic«'.  as  in  stajic  one. 

•  In  tlif  tliinl.  tho  kidney  is  (luito  roujih.  witli  numerous  |)in- 
point  projections,  yellow  re»l  and  purplish.  It  is  hard,  lolnilated, 
idinost  cart ilajiinou.s.  and  contracted." 

In  these  lesions  just  «piote<l  we  can  recojiiiize  thos<'  which 
iiiv  termed  to-<lay  acute  nephritis,  chronic  parenchymatous 
nephritis,  and  «'ontracted  kidney. 

I  nuist  now  touch  u|M)n  an  ini|M)rtant  |)oint.  which  you  nuist 
well  renjcmlK'r.  as  it  is  one  which  sul)se<juently  has  cau.s<'(l  a 
Hreat  deal  of  di.scussion.     Bri-jht,  from  the  start,  held  that  all 
these  three  stajies  were  of  uniform  character,  in  the  .sense  that  one 
advanc       to  the  other;  that  all,  then,  stood  in  temiH)rar>-  rela- 
tion to  each  other.     He  rejiarded  the  chan>:es  "  as  due  to  altera- 
tions in  the  circulations  of  the  kidney,  brought  about  by  in- 
fluences of  the  skin  and  stomach,  or  [noiiucimi  a  (hridally  in- 
Ihmitintonf  romlilioti  of  the  kidnvif."*     Hrijiht  did  not  think  that 
the  lesions  here  presented  were  the  only  ones  which  were  found 
in  the  kidney,  for  he  described  in  his  orijiinal  article  .several 
others,  which,  however,  were  rejiarded  a.s  of  minor  importance. 
The  ideas  of  Brijjht  necessarily  attracted  attention,  primarily 
in   Kn^dand,   and   were  taken   up  particularly   by  Christison, 
Osborne  and  Crejjory.''     Christison  separated  the  disease  itito 
acute  and  chronic  forms,  althoujih  he  held  that  it  was  e.ssentially 
chronic.     He  doubted  that  all  the  various  lesions  were  stages  of 
one  morbid  process,  but  left  the  exact  nature  of  it  undetermined. 
He  described  the  following  seven  different  chaufjes  in  the  kidneys: 

•  1  particilarlv  <iuoto  tl.is  stiit.-.n.M.t  of  HriRht's,  as  U'vl.-n  statos  that  tho  i<l.-ii  of 
inflainn.ati.m  l.a.l'.K.I  Ihti.  cxpn-sM-d  by  Hriitlu,  but  nitr.Ml.ir..,l  by  Ke.nl.anlt  an.l  hn- 
riclis.     An  I'vulciit  inistakcl 


8 


liliKillT  S    DISKASK 


1.  A  cotmcstion  of  the  kitlncvs  with  or  without  u:r;iniil:ir 
deposits  i;i  tlic  siil)sl;m('('. 

2.  True  ,<:r;iniil;ir  (l(>i:(Mi(M';ili(>n  of  ('orti(';il  or  tiilmlar  stnic- 
turc.     I'M   Finely  .;:r:iiiiil:ir,  (/'I   hotrvoidah 

o.  Dciiciicratioii  l>v  a  smooth,  lioinoiicnrous,  ycllowish-iiray 
mass,  iiit(M-mt'(liat('  in  consistence  between  tliat  of  the  liver  and 
the  lirain. 

4.   Disseminated  tuliercles. 

.").  Induration  of  semi-cart ilaiiinous  hardness. 

(>.  Atrophy  with  disapjx'a ranee  of  proper  renal  structure  and 
with  or  without  one  of  the  previous  morbid  states. 

7.  Simpl(>  ana'mia. 

lie  recognized  these  in  the  followiuir  stajies:  Incipient  sta<:e 
of  coiiiiestion.  or  reaction.  .Middle  stau;e  with  a  nearly  destroyed 
cortex.  .Vdvanced  staiic.  where  the  tubular  masses  were  (le- 
stroved. 

Christison  knew  that  the  di.s(>ase  tends  to  suppress  the  solids 
in  tlie  urine,  that  it  is  fre(|uently  associated  with  serous  inflam- 
mations and  severe  .-iiwemia.  and  emphasized  the  imprejination 
of  the  body-fluids  with  urea. 

On  the  other  hand,  some  oj)position  arose  on  the  part  of 
(ira\es,  lOlliotson,'"  and  Copland."  (iraves.'-'  particuhirlv,  re- 
<i.irded  the  kidney  lesions,  not  as  the  cau.sp  of  o'dema,  but  as  the 
result,  believin.ii  that  the  changes  in  the  kidney  were  .secondarj' 
to  an  effort  to  remove  the  (edematous  fluid  from  the  Ixxly. 

lurther  obscMvations  were  made  by  Willis.''  wh(i  was  the 
first  to  draw  attention  to  the  fact  that  all)uminous  urinr-  oc- 
curred in  a  munb"r  of  other  conditions  than  h;id  been  previously 
recounized. 

I'rom  Kuiiland  the  knowledjie  of  this  ^roup  of  diseases  spread 
to  France,  and  was  particularly  taken  up  by  Kayer"  and  his 
pupils,  rissot,''  Sabatier.'"  Desir.''  and  (ienest.'""     Hayer  pub- 


nisTouicAi.  iNTHonrcTiox  and  ci.assikication 


9 


lishcd  ail  extensive  v:iliial)le  monojirapli.  presentinjr  a  rich  ma- 
terial (»f  iiood  ohservatitms.  coiicludiiiji  that  liri.iiht's  tlisease  was 
an  innaininatorv  condition  of  the  ki(hiev.  essentially  charac- 
terizeil  hv  an  alhuniinous  urine.  c()ntainin,u:  less  salts  and  urea 
than  the  normal  and  always  associated  with  (edema.  He.shariily 
ditTereiitiated  it  from  other  forms  of  inflammation  which  he 
lii-ouped  as  rheumatic  nephritis. 

An  entirely  different  start  in  this  study  was  made  hy  Solon.'' 
He  collected  all  cases  of  "  alhuminuria,"  a  term  introduced  hy 
him.  and  tried  to  arrive  at  .some  conclusion  from  the  material 
thus  collected.  Hut  inasmuch  as  he  nece.ssarily  included  in  this 
iiroup  cases  of  all  sorts,  some  of  which  cimld  not  have  even  been 
kidney  diseases,  he  did  not  arrive  at  any  definite,  valuable  con- 
clusion. His  controversy  witli  Hayer  did  not  clear  the  matter 
any.  Solon  made  the  observation,  however,  that  the  symp- 
toms of  liramilar  kidney  frecpiently  differ  from  the  others,  par- 
ticularly in  an  ab.sence  of  codema,  but  were  associated  with  nau- 
.sea,  vomitinii,  and  pain. 

The  earliest  histolojrical  inve.sti^iations  into  Bri<:ht's  disease 
were  made  in  (lermaiiy  by  (ilujre,  Valenthi.  and  Hecht,  after 
Hecfiuerel-'"  in  France  had  exphiined  Brijrht's  disease  as  a  hyper- 
troi)hy  of  ^hllpi;Ihian  corpuscles,  which  he  re«>;arded  as  the  secret- 
iiifi  structures  of  the  ki(hiey.  But  because  of  a  very  insufficient 
and  somewhat  hypothetical  conception  of  the  finer  structures 
of  the  ki(hie>,  they  proved  of  little  conseciuence.  (lhi<ie-' 
rejiardeil  it  as  inflammation,  as  he  discovered  his  "characteristic 
inflammatory  jilobules,"  and  ^'alentin-- as  a  disease  of  the  blood, 
beinji  unable  to  find  any  characteristic  chans!;es  in  the  kidney, 
and  Hecht,-'  finally,  as  a  defjeneration,  analo-jous  to  his  opinion 
of  cirrhosis  of  the  liver.  ( ilu<ie  described  later  three  forms  of  the 
disease.  First,  one  of  inflainmation;  second,  a  cirrhosis,  which 
he  meant  in  a  literal  sense,  as  deposits  of  fat;  third,  an  "uiu-er- 


Id 


HKKillT  S    DISKASK 


tiiiii"  tl('ji(  iKMMtioii.     As  you   sco,  ;m   unsMtisfactorv,  (Icficieut 
(•l:l^si^i(•ati()ll! 

TIh"  liivat  anatomist  llciilc''  was  the  first  to  iiivc  a  conipre- 
liiMisivf,  roliahlc  dcscriptior.  of  the  liistoloiiv.  and  a  ^roat  many 
of  his  liistoloiiical  and  anatomical  descriptions  arc  considered 
correct,  even  at  tliepresiMit  day.  Me  reuiarded  tlie  wliule  proce.ss 
as  an  exudation  of  fil)rin  Ix'tween.  aiul  into,  the  tul)ules.  which 
oriianiz(>s.  contracts,  and  produces  a  cirrliosis  of  the  kichiey.  He 
employed  the  term  cirrhosis  in  the  modern  sense  of  coni'ective- 
t issue  formation  with  contraction.  Based  on  his  own  observa- 
tions ;ind  those  of  others,  he  differentiated  between  these  tyi)es: 

I.  Steatosis  (tf  the  kidney  ((iluue  and  Johnson). 

'2.  Subacute  inflanunation  with  cyst  forn-iation. 

'.i.  Cirrhosis  of  the  kidney. 

4.  Swelling-  of  the  kidney  due  to  (edematous  infiltration  and 
first  sta.iic  of  cirrhosis. 

.").  Acute  descpiamative  nephritis  followinu,  exanthemata 
(Johnson  i. 

The  lilomeruli.  in  his  opinion,  were  not  chanjied.  Ho  should 
l)e  particularly  reniemhered  as  heinsi  the  first  to  jiive  a  careful 
.lescription  of  tube  casts,  later  studied  thoroujihly  l>y  Xasse. 
Simon.  Scherer.  and  Hovida.  He  held  that  they  were  composed 
of  tii>rinousex\!date.  and  similar  views  were  entertained  by  \  ojiel. 

On  the  other  hand,  Canstatt.''  who  with  Siebold  had  studi(>d 
two  cases  of  the  disease,  reii;irded  the  lesions  as  either  a  non- 
inflammatory det)osit  of  albununous  fibrinous  uranules.  or  of  fat 
in  the  /ortcx:  a  "steatosis  renum.~' 

In  llntilaiid  there  appeared  about  this  lime  Bowman's  jiveat 
work  on  the  finer  structures  of  the  kiilney.  which  .uave  a  new 
impetus  to  the  study  of  Brijiiit's  di.sease.  Of  these  works, 
tho.se  of  Johnson,-"  Toynliee.-'  Simon.-'^  and  Busk"'  are  of  es- 
petial   importance.      In  these  investigations  there  appears  for 


IIISTOKICAI-    INTHOOrCTION    AND    CI-ASSIKICATION 


11 


tho  first  time  an  eiuloavor  tohold  difforeiit  procossos  rosponsiblo 
for  the  syiiiptom-coinplex  and  charactoristic  features  of  Brijiht's 

disease. 

Toyiil)ee  was  tlie  first  to  describe  the  thickeninjr  of  the  arter- 
ies, and  interstitial  celhilar  proliferation,  'v'lile  Johnson  paid 
particular  attention  to  the  fatty  infiltration  of  the  tubular 
epitheliutn.  leadinji  to  what  he  called  a  chronic  des(|uaniative 
nephritis.  He  held  that  th's  may  develop  independently  without 
previous  acute  chan^'es,  and  therefore  was  one  of  the  first  to 
discard  the  uniform  view  of  Brijiht's  disease.  He  reeo}>;- 
nized.  further,  amyloid  and  fatty  kidney,  iiusk's  idea  was  that 
the  contracted  kidney  resulted  from  a  capillar>-  phlebitis,  as 
granular  liver  results  from  a  portal  thr(mibo-phlel)itis. 

Important  coiitril)Utions  appeared  in  works  of  Reinhardt '" 
and  Frerichs."  Keinhardt  re<rarded  the  lesion  as  a  difjut^e 
injinmmntion  with  a  i>eculiar  hick  of  organization  on  the  part  of 
the  fibrin,  and  leadinji  to  a  destruction  of  the  epitheliimi. 
Krerichs.  extendinji  these  views,  distinjjuished  between  the  fol- 
lowiiifi  al)S()lutely  correlated  stajies:  First,  hyperiemia  and 
l)e<iiiuiin.ii-  exudation;  .second,  exudation  and  metamorpho.sis  of 
the  exudate;  third,  rejjression  and  atrophy,  in  which  the  exudate 
may  be  partly  transformed  into  connective  tissue.  This  classifi- 
cation came  into  jreneral  use  before  Virchow.  On  the  other 
hand.  Hockitansky.'-  a-rain  separated  exudative  nephritis  en- 
tirely from  Bri-iht's  disease  and  regarded  as  characteristic  of 
that  lesion  a  ilegeneration  and  descpiamation  of  the  ei)ithelium. 
But  he  allowed  a  possil)le  combination  of  Bright's  disease  with 
n(>phritis. 

We  come  now  to  a  very  important  turning-point  in  the  history 
of  Bright's  disease,  as  well  as  in  the  whole  history-  oi  pathology. 
In  lSo2  Virchow"  published  a  celebrated  article  in  the  fourth 
volume  of  his  "  Archives,"  on  "  Parenchymatous  Inflammation." 


12 


UHKillT  S    DISKASi; 


lie  WMs  the  first  to  use  lliis  term,  which  since  then  h;is  hccomc 
coinnum  property.  In  it  he  hiid  the  corner-stone  for  ;ill  future 
idens  ;il)out  parencliyiuiitous  inn.MUUUMtion.  ;ihhouiih  you  will 
|)resently  see  th;it  N'irchow's  ideas  of  parenchymatous  inflamma- 
tion are  entirely  dilTeicnl  from  what  was  later  reuarded  as  such. 
It  may  therefore  he  necessary  to  detail  some  of  his  views  in  that 
relation. 

Before  the  time  of  N'irchow.  the  ideas  of  inflammation  may  he 
uained  from  N'oirers definition : "  Inflammation  capillary  hyper- 
M'lni;!  :  hydrops  tihrinosus."  \'irc'!ow's  ohservatior.s  led  him  to 
the  conclusion  that  it  was  (>rroiieous  to  reuard  the  exudate  as  the 
essential  features  of  any  inflanmi.ation.  hut  that  the  constant 
char.icteristic  of  inflammation  w.is  parenchymatous  tlejiener- 
ation.  This  resulted  from  an  excessive  imhihition  of  e"  "ded 
fluid,  which  lie  rejiarded  as  exaiiiicrated  nutritive  materia!  It 
led  him  to  the  idea  that  the  inflammatory  process  was  really  a 
nutritive  disturhance  of  parenchyma  cells,  and  he  ajiplied  this 
view  particularly  to  the  kidneys.  .\s  the  re.sult  of  this  excessive 
nutriment  the  cells  heconie  larjje  and  .swollen,  and  the  alhuminotis 
molecular  contents  are  increa.sed.  Thus,  he  as.s(nned,  the  pro- 
toplasm (>f  the  cell  disinteiirates  and  hecomes  fatty  and  jirauular. 
In  some  cases  the  whole  of  the  exudate  is  thus  consumed  hv  the 
epithelial  cell,  so  that  the  fil)rin  does  not  appear,  and  the  only 
evidence  of  the  presetice  of  the  exudate  is  fotmd  in  the  alhumin 
which  is  carried  ofi"  in  the  urine.  Virchow,  then,  rejiardod  the 
parenchymatous  chanjie  as  the  essential  feature  of  every  in- 
flammation, and  this  disturhance  of  mitrition,  as  he  termed  it, 
differs  from  simple  dejieneration  only  in  dejiree.  He  concludes 
with  the.se  words:  "I  vindicate  ahove  all  the  dejrenerative 
character  of  inflammation,  and  althou<rh  I  reuard  it  as  increased 
nutritive  pheiu'  ..enon,  I  do  not  see  in  it  an  evidence  of  inercased 
strenjith,  hut  an  expression  of  its  dimiiuition." 


HISTOHUAl.    INTKODICTION    AM)    CI-ASSIKICATION 


13 


(iuided  by  these  considerations,  he  (Hstin<iuished  iK^tweon 
three  forms  of  nephritis,  for  which  he  created  tlie  following 
terms,  which  are  still  employed  to-<lay,  althoiijih.  as  you  will 
appreciate,  in  a  different  sense  from  the  one  Virchow  <iave 
them. 

First,  catarrhal  inflammation,  wliere  cells  become  jiranular, 
opaque,  and  l)reak  off  the  basement  membrane. 

Second,  -roiipous  inflammation.  Here  the  cells  show  es.sen- 
tially  the  same  chanjies,  but  become  mixed  with  a  coajiulated 
hl)rin()us  exudate. 

Third,  true  parenchymatous  inflammation,  which  is  the  most 
intense,  and  consists  of  a  jrranular  swellin;;-  and  disintejiration 
of  cells  with  the  formation  of  a  soft  detritus 

Niemann,  one  of  Virchow's  pupils,  in  his  inaufjural  disserta- 
tion 1 1.S4SI.  jiives  the  following  interest injr  and  excellent  descrip- 
tion of  the  finer  {)arenchymatous  changes  in  nephritis  in  Vir- 
chow's sense:  "  (Jui  ijuiden  processus  (Infl.  parenchymatosa )  in 
renibus  procedit.  et  (luiden  maxime  in  epithelii  cellulis  canali- 
culorum  uriniferorum  contortorum  in  substantia  corticali. 
lOpithelii  celluhe  majores  Hunt,  c/if/o.smo.s/.s  niirta*  eorumciue  con- 
tentum  mol)ilum  turl)idum<jue  fit.  Cellulis  autem  amplificatis 
canaliculi  uriniferi  extciuluntur  et  renum  aml)iturf  major  existit. 
Caiialiculorum  amplificatione  circuitiis  sauiruinis  in  vasis  capil- 
laribus  impeditur.  undc  ana>mia  renum  oritur,  in  renum  super- 
ficie  astra  venosa  conspiciuntur,  (piia  sanguis  venosus  refluere 
n(>(iuit. -Turn  celluhe  ilhe  metamorphosin  adiposam  .subeunt, 
emollivmtur,  deniipie  massam  formant  pultiformem,  (pue  urinie 
admisceri  potest,  (pio  urina  fit  adiposa.  ilmv  quidem  admixto 
raio  fit.  plerum(iue  massa  iUa  resorbetur.  Processu  progrediente 
canaliculi  uriniferi  collal)untur.  (piai  in  renum  superficia  loca 
tlepressiora    formautur   et    renes   speciem   granulosam   pne   se 

•  llalii's  iniiu'. 


14 


HIJKiHT  S    DISKASK 


fcruiit.     Loca   data    in    rciuim   snpcrficia    coloro   intense   flavo 
|)()rt(>s  sunt.  (|iue  nietainnrpliosin  adiposani  non  suhierant." 

lie.  theretore.  classities  the  lesion  in  tli(>  three  previously 
detailed  stages.*  It  is  interest inir  to  recall  here  that  Virchow 
sharply  dilTerentiated  the  cicatrieial  formation  as  the  result  and 
not  as  part  of  the  inflanunalory  process.  Wv  will  learn  that 
such  a  stand  has  only  receiuly  been  taken  ajiain  by  .XscholT. 

Ill  IS.")!*  Arnold  Heer.  a  |)upil  of  Virchow.  stinnilated  by 
Hownian's  and  (ioodsir's  work.  |)ul)lished  a  inonojiraph  on  the 
eoiuiective  tissue  of  the  human  kidney  in  health  and  disease." 
In  this  he  paid  |)articular  attention  to  the  inter.stitial  hyperpla- 
sias in  various  forms  of  nephritis,  which  he  carefully  described, 
alone  and  iti  connection  with  the  accompanyinif  vascular  and 
parenchymatous  ehan<:es.  It  is  interesting!;  lo  note,  in  view  of 
Weiiicrt's  later  work  and  ideas,  that  he  inclines  to  the  belief  that 
atrophy  of  tul)ules  and  jih)meruli  prec-edes  the  connective-tissue 
hyperplasia,  and  that  the  process  is  more  or  less  of  a  peculiar 
complementary  character,  i  Pp.  110  and  122.)  Interestinji  is. 
further,  that  he,  as  the  first,  attaches  considerable  sijinificanco 
to  the  proliferation  of  the  epithelium  in  nephritis  (p.  12")).  which 
explains,  in  his  opinion,  that  kidneys  may  show  microscopically 
.small  atrophic  glomeruli  and  appear  <iranular,  l)Ut.  at  the  same 
time,  as  a  whole,  are  of  normal  size  or  even  enhirjied.  The 
tuiniles  in  these  cases  appear  dilated  .and  filled  with  hyper- 
pla.stic  epithelium.  I'uture  invest ijiat ions  have  unfortunately 
disreiiarded  this  important  process  of  the  lesion. 

Beer  was.  therefore,  the  first  to  draw  the  interstitial  coimec- 
tive-ti.ssue  chanjres  prominently  into  the  discussion.  When  it  is 
further  considered  that  shortly  afterward  appeared  Cohnhenn's^' 
classic  ol)servations  on  inflammation,  which  aj^ain  placed  the  es- 
sential featuresof  that  proce.ss  in  and  around  the  vascular  system, 

•('itc(l  iiftcr  Virt-liow. 


mSTOHICAL    INTUODICTIOX    AM)    CI-ASSIKIfATIOX 


15 


Mild  which  oxcitod  a  jircat  iiifluoiico  on  all  contpmporary  invest i- 
sratois,  it  hccojncs  appr<'cial)l<'  how  the  attention  contorcd  once 
more  around  these  chanjres.  This  influence  is  well  shown  in  tlio 
works  and  etTorts  of  Traul)e '"  to  differentiate  between  a  cir- 
cuniscapular  and  intertvihular  nephritis,  and  to  nejilect  the 
parenchynititous  involvement.  The  subsequent  establishment 
of  <ilomerulonephritis  as  a  special  tyiK>  by  Klebs,'"  and  which 
was  later  rejiarded  by  Hibbert'''as  the  universal  incipient  lesion 
of  all  forms  of  Brijiht's  disease,  broujiht  equal  support  to  the 
prominence  of  the  vascular  and  interstitial  chanjies. 

However,  it  remains  Traube's  fjreat  merit  to  have  conclu- 
sively separated  the  cyanotic  and  amyloid  kidneys,  as  non- 
inflannnatory,  from  nephritis. 

These  views  of  the  pureh'  vascular,  interstitial  inflammator>- 
nature  of  nephritis  did  not  entirely  succeed  in  replacin<>;  Virchow's 
conceptions.  As  in  other  scientific  discussions  where  both  sides 
of  an  ari^ument  contain  truth,  both  were  accepted,  but  un- 
fortunately as  distinct  and  different  types  of  nephritis,  and  it 
became  prevalent  to  speak  of  parenchymatous  and  interstitial 
i\ephritis  in  a  contrast in<i  sense. 

This  created  a  very  jrrave  and  fundamental  error  from  which 
pathology  is  still  sufferinjj;  to-day.  It  was  based  entirely  on  the 
too  narrow  definitions  of  inflammation  of  \'irchow  on  the  one 
side,  and  of  ("ohnheim  on  the  other. 

It  was  Hosenstein"'  who  first  endeavored  to  establish  a 
reconciliation  Ix'tween  the  two  extreme  views  of  parenchymatous 
and  interstitial  inflammaticm,  inasmuch  as  he  rejrarded  epithelium 
as  well  as  interstitial  tissue  involved.  He,  therefore,  advocated 
the  term  and  idea  of  diffuse  nephritis,  ori-rinally  introduced  by 
lieinhardt.  and  further  emphasized  that  one  should  differentiate 
between  de<reneration  and  inflammation.  Herein  is  expressed 
an  actual  chanjie  in  the  ideas  of  the  character  of  inflammation,  as 


16 


UHKillT  S    DISKASK 


('ss(Mili;illy  ifprcsciilcd  l>y  the  curlier  writers  and  also  by  Cohn- 
heiin  ami  Nircluiw.  Whereas  these  <-()iisi(lere(l  an  inflammation 
only  as  an  exudation,  and  Virchow  essentially  as  a  de<ienerati(m, 
Kosenstein  inten(h'(l  to  coinliine  hoth  as.  not  necessarily  depen- 
dent. Imt  correlated  processes.  The  uncertainty,  however,  on 
all  <|Uestions  here  discussed  was  particularly  well  .shown  in  the 
discussion  of  lirii:ht's  disease  at  the  first  meetinjiof  the  (lerman 
Coiiiiress  for  Internal  Medicine  in  ISS2.  wh/MV  Leyden."'  for  in- 
stance, held  th.at  all  cases  with  alltuminous  urine  and  anasarca 
should  iK'urouped  as  Briiiht's  disease,  while  all  others  were  to 
he  regarded  as  n(>phritis.  This,  of  course,  included  the  non- 
iiiflannnatory  amyloid  in  the  cate^'ory  of  Hri^rht's  disea.se.  while 
a  contracted  kidn(\v  without  cedema  and  albumin  was  to  he  ex- 
cluded.    A  perfectly  untenable  position! 

In  I'.n^land.  further  studies  gradually  led  away  from  the 
orijLiinal  id<  as  of  Hrij-ht.  After  ("hristison  and  Johnson  had 
doul)ted  the  intim.ite  relationship  of  all  forms  of  nephritis,  voices 
in  that  direction  became  stronjrer.  Particularly  Sanmel  Wilks^' 
renarded  the  lariic  whit(>  kidney  and  small  «iranular  kidney  as 
independent  .-itYections.  followed  by  (Irainjier  Stewart,'"'  .'"id  in 
ISTlMiuU  and  Sutton  "  went  so  far  as  to  declare  that  artoriiil  and 
capillary  fibrosis  was  the  cause  of  ccntracted  kidneys. 

In  (lermany.  liart(>ls"  was  the  first  to  introduce  the  idea 
of  the  independent  chanicter  of  the  so-called  chronic  interstitial 
nephritis  which  he  attrilmted  to  a  primary  jirowth  of  interstitial 
tissue,  lie  distlii,miished  it  from  the  so-called  parenchymatous 
form. 

Senator.''  however,  ajiain  drew  attention  to  the  point  that 
a  sharp  division  bef..<en  these  so-called  chronic  parenchyma- 
tous and  interstitial  forms  was  not  })o.ssible.  and  that  one 
oujiht  to  speak,  as  Heiiihardt  and  Kosenstein  had  done,  of  diffuse 
nephritis.     At  the  same  time,  he  admitted  that  there  exists  a 


IIISTOHICAI,   IXTHODICTIOX    AM)   (l.ASSIKKATKt.N 


17 


form  of  nephritis  distinct  from  the  onliniiiy  interstitial  ty|)e,  in 
the  artcriosclorotic  kidney. 

The  modern  turnin<!:-|)oiiit  in  the  sulgecl  of  nepiwitis  may  he 
properly  said  to  i-ommence  with  the  observations  of  Weifrert,'" 
wiiicli.  like  N'irchow's,  are  important,  not  only  from  the  stand- 
poii.l  of  ki<lney  patholojiy,  hnt  in  a  nnich  more  jieneral  sense. 
Weifierl  very  stronj-iy  advocated  a  uniform  view  of  all  kidney 
lesions,  and  claimed  that  a  sharp  line  between  the  various  forms 
could  not  lie  drawn,  and  that  they  represented  only  (plant itative 
(lin'erences.  Mis  most  radical  idea  expressed,  however,  was  that 
the  interstitial  inflanunatoiT  and  productive  ciianjres  are  always 
secondary  and  caused  by  a  parenchymatous  destruction  or  loss. 
This  idea,  which  has  become  widely  adopted,  is,  as  you  appreciate, 
the  very  opposite  of  Virchow's  conception.  It  marks  the  time 
when  parenchymatous  inflanunation  bejian  to  be  rejiarded  in  an 
entirely  different  sen.se  fnmi  that  of  the  orijiinator.  Parenchv- 
m.itous  dejieneration  became  no  more  a  nutritive  disturbance, 
but  the  result  of  an  irritant,  and  the  direct  expressicm  of  its  in- 
jury. It  is  this  conception  of  parenchymatous  de<i;eneration  which 
rules  to-day. 

\\'hile  W'eificrt  held  this  op[)osin^  view  to  Mrchow,  he 
nevertheless  broujiht  parenchymatous  dejieneration  in  a  direct 
pathojicnetic  relation  to  the  interstitial  chanj^es,  and,  as  I  shall 
h!iv(>  occasion  to  nie'ition  immediately,  the  present  fjeneration 
does  not  attach  any  more  patho^eiietic  sijinificance  to  these 
terms. 

Weijiert  distinuuished  l):'tween  four  intimately  correlated 
forms:  Acute  nephritis,  characterized  mainly  by  cellular  exu- 
date; the  (subchronic  nephiitis.  characterized  by  bejiinninft 
coimective-t issue  <j;rowth;  the  chronic  nephritis,  characterized 
by  a  be«iiimin<i  contraction;  and,  lastly,  the  firanular  atrophy, 
characterized  by  a  very  comj)lete  loss  of  parenchyma. 


If^ 


IS 


HUKillT  S    DISi; ASK 


llicsc  idcMs  (if  Wfbcil  were  JiiiMin  sliitii;rly  (i|)|m>s<'(I.  iiimiiiIv 
l)v    Zif'dcr,"    .\;iu\V(Mck.'^    Miiilcls."   :iii<l.    to   some   drurw.  I)y 


St'iiiilor. 


Njiiiwcnk.  p.irticiil.irly.  drew  iittciitioii  to  the  fact  tliat  the 
(l«'In'inl<Mi('c  of  till'  iiitnsiitial  cliaiiucs  on  the  parciicliymatous 
(lest iiii't ion  call  liv  no  means  Kc  always  dcMionstratcd. 


Z 


iciiicr 


foil 


o\\> 


w 


('1"<'II    III  so 


far  :;s  ln>  also  takes  a  uniform 


view  of  all  lia-matojii'iious  forms  of  nephritis,  helieviiij;  only  in  a 
•iiaded  and  no  essential  dilTereiice.  That  it  is  jiossihle  to  difTer- 
entiate  strictly  lietwein  deucnerations  and  inflammations  is 
denied  l»y  Zienler.  In  opposition  to  Wei-icrt.  following  Hartj'ls. 
he  descrilies  a  primary  interstitial  nephritis,  the  result  of  a  pri- 


ma 


ry  connective-tissue  hyperplasia,  leading  to  induration. 

'I'liese  views,  opposing  Weijicrt's  conclusions,  found  furtlier 
support  in  certain  observations  on  the  so-called  acute  interstitial 
nejihritis,  as  first  descrilKHl  by  liiermer. ''  Mrnst  Warner.'-  Klehs,"'' 
and  lately,  with  particular  c:ire,  by  Councilman.''  Tlie  latter  re- 
•rards  this  lesion  as  a  foail  infiltration  by  plasma  cells,  derived 
from  emigrated  lymphocytes;  but  this  cannot  find  its  explana- 
tion in  a  primary  epithelial  dejreneration,  which  is  always  tlilJusc. 
When  tlie  latter,  however,  becotnes  intense,  polynuclear  leuko- 
cytes are  attnicted,  and  not  plasma  cells.  He  arjiues.  therefore, 
that  the  interstitial  exudate  is  primary  and  accompanied  by,  but 
not  dependent  upon,  epithelial  destruction. 

With  this  battle  of  opj)osin<i  ideas  .still  pendinj:,  a  further 
complication  arose  in  a  jiradual  chanjie  in  the  meaninji;  of  the 


terms  parenchymatous  anc 


I  interstitial  inflanunations.     This  is 


perhaps  liest  illustrated  in  Orth's  po.sition  on  the  .subject. 

Orth  '  recojiiiizes  primarily  a  parenchymatous  and  interstitial 
nephritis,  by  which  he  means,  however,  pmloniimttimf  chaHiifs  in 
parenchymatous  and  interstitial  ti.s.sue  respectively.  He  uses 
thcxc  (cnnx,  thnjorc,  piirihf  in  a  ilt.scrij)tive  sense,  and  not  in  any 


HISTOUICAI,   I.\TIU»l)r<TI(>N    A\l>   <I,ASSIIMATI(>X 


19 


IMtthiuji  iirtif  niaininif.     In  this  iilrtt  the  hinitst  niutil»r  oj  jxilholo- 
illsts  ittitl  rliiiirinns  at  jiirscnl  conntr. 

As  ;i  sitlxlivisioti  and  iiitcniu'diary  form  ln'  rrjianlM  jflo- 
mcniloncpliritis.  \lv  .states:'"  "It  has  \m>u  attctnptcd  from 
varu)iis  sourros  to  ('stal>lisli  a  uniform  view  for  all  the  uon- 
piinil.'iil  nephrites,  iiiasmueh  as  some  h(tl(l  that  the  parenchyma 
cells  are  always  primjrily  involved,  others  that  all  commence 
with  a  jilomerulonephritis.  I  caimot  ajiree  with  one  or  the  other 
opinion;  in  fact,  with  no  exclusive  view  at  all.  .\s  far  as  I  can 
see.  a  uniformity  exists  only  in  so  far  as  any  inflanunatory  irri- 
t.inl  chanjies  vessels  as  well  as  tis.sues,  hut  I  hold  it  justifiahle  to 
speak  of  various  forms  of  kidney  inflanunation,  because  the  dif- 
ferent constituents  of  the  kidney  are  concerned  in  a  most  unecpial 
manner.  Followin<r,  therefore,  the  principle  'a  potiori  fit 
denominatio,'  I  jro  .so  far  as  to  acknowledj^e  a  parenchymatous, 
interstitial,  and  jilomerulonephritis.  But  it  must  he  remem- 
l)ered  that  no  .sharp  line  of  demarcation  hetween  them  is  pos.sil)le. 
and  that  their  coml)inations  are  frecjuejit  findin<ts."  In  this 
sense  he  de.scrihes  a  productive  parenchynuitous  and  a  productive 
interstitial  nephritis,  of  acute  ami  chronic  variety. 

The  ideas  of  Senator"'"  have  apparently  heen  most  widely 
adopted  hy  clinicians.  lie  holds  that  the  differences  in  the  forms 
of  nephritis  depend  ujion  the  course  and  the  duration  of  the 
disea.se.  and  they,  in  turn,  upon  the  intensity  of  the  irritant.  The 
stronjier  the  latter,  the  more  diffuse  and  extensive  the  involve- 
ment. The  weaker  irritant  finds  expression  only  in  parenchy- 
matous attack  (tubules  and  ftlomeruli),  while  the  interstitial 
tissue  shows  only  hyperspmia.  An  acute  interstitial  nephritis 
without  parenchymatous  chanjje  is  denied  hy  Senator. 

He,  therefore,  differentiates  hetween  an  acute  parenchymatous 
(in  the  sense  of  Orth)  and  diffuse  nephritis.  Strictly  sjx'akinfi, 
a  chronic  j)arenchynuitous  nephritis  cannot  exist,  inasmuch  as 


i 


I     ' 


2<» 


lUIHiHTs    DIHKAHK 


lc;i(liiii;    l<»    iiidiirMtidii.     Clinmic    forms    of    ncithiilis 


after  a  tiiiu'  llic  iiilcrslitial  tissue  heeoiiios  always  involved;  lait 
S<"iiator  holds  thai  term  admissil.le.  to  si'iiiify  that  these  ehaiines 
are  primarx  and  most  prominent.  Hut  he  disa^irees.  as  pointed 
out  Iwi'ore.  with  Wei^ert  as  to  whether  parenehvinatoiis  de- 
i:eiieralion  must  alwaxs  preicde  thi-  intj'istitial  chanv:!'.  He 
holds,  moreoxer.  that  clironie  inflammations  of  the  coniu'ctive 
tissue  are  rapidlx  followed  l>v  de^icneratioii  on  part  of  tln'  paren- 
eh\  II 

result  either  from  a  previous  acute  condition  or  may  develop 
inde|)eii(iently.  Chronic  nephritis  may  also  result  from  arterial 
chaiiucs  in  the  kidne> .  leadinj:  to  atrophy  of  ^ilomeriili  and 
liilmles.  I'inally,  any  of  these  chronic  types  may  at  any  time 
under^io  acute  exacerl  tat  ions,  producinji  new.  very  variable, 
anatomical  and  clinical  pictures. 

.Vt  a  recent  discussion  of  the  (lerinaii  Patholojrical  Society. 
Midler  ^iirain  has  revived  the  discussion  about  the  impos.sil)ility, 
even  clinically,  of  ditTerentiatinjr  between  acute  and  chronic 
nephritis,  and  the  erroneous  conce|)tion  implied  in  .s|H'akinv;  of 
parenchymatous  nephritis,  because  the  lesion  is  always  diffuse 
a^'d  the  interstitial  tissue  as  much  invohed  in  the  process  as  the 
parenchyma,  even  showinj;  de>i('n«'rative  ciianjies  in  the  form  of 
fatty  infiltration  Lolileim.  .\uain.  in  the  so-called  interstitial 
forms,  it  would  be  erroneous  to  believe  that  the  parenchyma  was 
noi  much  involved  and  <lisiiite^iated.  for  glomeruli,  as  well  as 
tubules,  show  severe  chaiiLics.  lie  further  drew  attentiofi  to 
the  difliculty  of  any  satisfactory  ("tiolojiical  clas.sification;  and 
j:rouped  ofT.  much  as  formerly  was  done,  dejienerations  from  true 
inflammation  of  the  kidney,  and  recommends  jiirouping  them  as 
nephroses,  as  contrasted  with  nei)hritis. 

Finally,  we  must  rciiard  the  ideas  of  L()hlein,"''^  which,  comin<r 
from  Marchand's  Institute,  represent  mainly  the  ideas  taujiht 
there.     Me  also  believes  that  in  maiiv  cases,  which  involve  almost 


IIIST()HI<AI.    INTHOIHTTION    AND   CLAMSIKKATION 


21 


«'X('liisiv«'ly  the  n'ual  parcuchyina,  as  in  thc>  lesions  prodiircd 
liv  cholera,  syiianclH'.  |K»isoninns,  pn'^nancy,  etc.,  there  exists 
MO  real  iiifiaounation.  Itiit  a  (iejieneration,  which  has  a  ^reat 
tendency  to  Iwal.  and  prolialtly  almost  always  heals  eoni|)let(>ly. 
'l"he  true  nephritis  is  infianiinatory  and  has  its  prntotyix'  in  the 
;rloiiierulon(>phritis.  The  |)arenchyinatouH  ehan>ies  thej-e  de- 
|M-nd  mainly  n|M)n  the  glomerular  ones  in  their  intensity  and 
duration.  Acute  interstitial  nepliritis  must,  howev<'r,  1k'  con- 
sidered in(le|M>ndent.  Chronic  nephritis  with  hydrops  n'sidts 
fn»m  all  cases  of  jtlomerular  nephritis  which  do  not  heal,  or 
may  commence  insidiously  without  acute  manifestation;  in 
reality  they  reprt»s<'nt  the  results  of  an  acute  nephritis. 

Lastly,  the  secondary'  contracted  kidney  always  presents 
anatomical  evidences  of  a  ^tlomerular  nephritis,  which  may  he 
traced  to  piwious  acute  lesions.  It  is  certainly  more  frtHjuent 
than  sup|K>sed.  In  some  of  these  cases  the  featun's  an*  so 
characteri.stic  that,  without  knowledjie  of  the  previous  history 
of  the  individual,  the  diajinosis  of  nephritis  can  l)e  made. 

In  this  connection  L(>hlein  emphasizes  a  ty|)e  of  case  which, 
havin<!;  passed  throUfih  an  attack  of  acute  nephritis  with  hydrops, 
enjoys  relativ"  health  for  .some  time,  then  .suddenly  dies  with  all 
the  symptoms  of  nepliritis.  Here  is  frecjuently  found  a  typical 
chronic  glomerulonephritis  with  .severe  contraction  of  the  orjian. 

This,  <:entlemen,  is  an  outline  which,  although  incomplete 
and  ne<;lectin<t  much  and  the  works  of  many,  seems  to  me  to 
contain  the  salient  disputed  points.     What  may  we  conclude? 

With  re^iard  to  the  (piestion  as  to  what  to  include  under  the 
fi<'neral  headinji  of  Bri}!;ht's  di.sease,  I  think  it  has  jiradually 
develojM'd  to  limit  its  application  to  the  non-specific,  haemato- 
jrenotis.  non-purulent  inflammations  of  the  kidney,  and  we  may 
exclude  from  it,  therefore,  all  non-inflammatory  affections,  par- 
ticularly the  chronically  con<j;e8ted  kidney  and  its  after-results, 


i 


•)•> 


UKKillT  S    DISKASK 


fiirllicr  Minyloid  and  fatty  iiiiiltratioiis.  and.  as  will  appear  lator, 
the  senile  at ropliy  of  the  kidney.  Specific  inflaniiualory  lesions 
of  known  etioloiiy  or  riiori)liolo.uy  have  also,  hy  virtue  of  their 
characteristic  etiology  and  niorpholoiiy,  lie(>n  elinnnatod.  as  well 
as  ascendiiiii  inflammations  from  the  bladder. 

1  say  that  this  opinion  is  uradually  jiettinj:  the  upper  hand; 
some  seem  to  think  that  parenchymatous  dejienerative  lesions 
should  enjov  an  independent  recounition  amonji'  inHanimat(.ry 
changes.  To  these  invest iiiators  the  term  Hrijilit's  disease 
appears  still  indispensable  as  a  more  jiCMieral  one  than  nephritis. 
I  caimot  aiiree  to  that.  for.  whatever  theoretical  considerations 
mav  form  the  foundation  of  that  idea,  and  1  consider  them  very 
sliiiht  indeeil.  |)ractically  we  not  only  iiain  nothinu;  hy  this  fine 
line  of  ilemarcation.  l)Ut  it  forms  the  source  of  endless  confusion. 
I  shall  ipialify  my  position  in  this  matter  more  fully  later. 

Tlu'  term  nephritis  will  therefore  l)e  used  in  the  followinjr 
discussions  as  synonymous  with  and  instead  of  Brijiht's  di.«ea.se, 
liecause  it  has  a  ceilain  definite  meaninji  and  caimot  lie  misunder- 
stood. We  caimot  ajiree  as  easily,  and  will  pnthahly  meet 
mui'li  ,i:r(>ater  opposition,  in  dehiiini;  our  position  on  the  second 
and  most  important  point:  namely.  What  are  the  characteristic 
features  of  this  inflammation?  and,  sulKsetpiently,  how  the 
vaiious  inilammatory  processes  in  the  kidney  may  he  ade- 
(piately  classified. 

Here  you  must  well  reniemher  what  we  reviewed  ;i  .short  while 
a^o.  The  terms  parenchym.itous,  interstitial,  diffu.se,  persist  like 
threads,  hut  of  ev(>r-chaniiin.ii:  colors  throuiihout  the  historic  de- 
velopment of  infiannnation  in  general,  and  nephritis  in  particu- 
lar. I  hold  that  the  sooner  we  iireak  with  their  use,  the  hetter 
for  the  progress  of  kiiowledjic  hut  particularly  for  our  under- 
standinji  of  inflanunatory  phenoiiema  and  that  of  nephritis. 

We  have  seen  how  the  views  of  \'i'"cliow.  Beer,  Cohnheim, 


UISTOKICAI.    INTUODICTION'    AM)   Cl.ASSIKICATlON 


Zi 


Wciircrt.aiul  others,  iiftor  whom  the  words  parcncliyiiiatous  and 
interstitial  iiiflaininatioiis  were  employed  in  a  strictly  patho- 
jiciietically  contrast inji  sense,  have  not  been  upheld  hy  future 
invest i;rat ions.  It  is  undeniable  and  clear  that  certain  inflamma- 
tot  v  initaiit!  atl'ect  extensively  and  perhaps  primarily  the 
ep  helium  in  (lc':,('neration  a'ld  j)roliferation,  and  that  there 
an  itliers  wliicii  similarly  involve  the  interstitial  and  vascular 
system  in  exudation  and  production.  Both  are,  however, 
always  comhined.  correlated,  and,  at  least  after  a  short  time, 
ecjually  afl'ected,  so  that  in  ;iny  established  inflammation  in 
other  words,  in  any  nephritis  a  differeiitiation  between  par- 
enchymatous and  interstitial  inflammation  becomes  practically 
impossible.  Hut  with  the  pathojienetic  meaninji  of  these  terms 
lost,  tlieir  em{)loyment  is  no  more  justihable,  for  I  cannot  even 
aiiree  that  these  terms  may  be  u.sed  in  a  purely  descriptive  sense. 

Aside  from  th(>  fact  that  it  does  not  seem  wise  to  me  to  con- 
tinue terms  in  an  arbitrary  other  .sense,  which  is  bound  to  pro- 
duce return  to  coiifiisiou  instead  of  an  advance  to  jireater  clear- 
ness, this  nomenclature  has  not  even  exactness  in  its  favor. 

We  have  learned,  you  remember,  that  many  changes  which 
some  have  predominantly  related  to  the  parenchyma,  are 
eijually  well  and  -severely  represented  in  the  interstitial  tissue 
(fatty  dejieneration  and  inflannnatory  o'demai.  Ajiain,  in  the 
.so-called  typically  interstitial  lesions,  <;lomeruli  and  epithelium 
of  the  tubules  are  exten.sively  affected  antl  destroyed,  ^^'ho 
could  state,  therefore,  which  were  more  affected  in  one  case  than 
in  the  other?  Such  an  opinion  can  be  based  only  on  very  su- 
perficial examination  of  disea.sed  kidneys. 

iMpially  objectionable,  finally,  are  the  two  terms  acute  and 
chronic,  for  they  not  only  do  not  describe  with  any  de<tree  of 
precision  the  time  limit  of  a  nephritis,  or  the  rapidity  of  its  forma- 
tion and  its  pro<:ress,  but  they  have  lost  in  the  course  of  patho- 


ii 


'» 


MKKiHT  S    DISKASK 


loiiical  iincstiuMtioiis  niiy  definite  siuriiticaiice  with  reiijinl  to  a 
p;ir(iciil:ir  process  or  uioiip  of  processes. 

As  Miiiler  li;is  pointed  out.  tlierefore,  tlie  terms  acuie  and 
chronic  liave  even  lost  tnndi  of  their  chnicdl  ineaninj;-.  When 
does  an  acnte  nephritis  lu'conie  chronic?  Here  is  (oo  much  room 
for  indivi(hial  opinion  .ind  discussion.  .Moreover.  ki(hievs  are 
found  at  autopsy  after  short  iUness.  showinji  lesions  of  a  character 
now  iirouped  as  typicall}'  chronic;  and,  ajiain,  after  lonji-con- 
tiiHied  ilhiess.  showiuii  predominatinji'  clianjj;(>s  of  so-called  acute 
character. 

Xothinu  at  all  is,  therefore,  ;>ained  for  the  understandinji  of 
the  })athoiojiical  process  l)y  th(>  terms  acute,  subacute,  and 
chronic:   they  may  even  actually  mislead. 

For  all  these  reasons,  and  to  further  progress  in  our  knowledj^e 
of  the  inflannnatory  lesions  of  the  kidney,  I  propo.se  to  di.scard 
all  these  terms,  which,  on  account  of  the  many  ways  in  which 
they  may  he  intended  to  apply,  have  and  always  will  he  the 
ureatest  source  of  confusion,  and  a  drawhack  to  ;i  hetter  under- 
standinu  of  pathol- uical  conditions. 

1.  The  term  nejjhritis.  which  in  itself  means  inflammation  of 


the 


kid 


nev, 


nd   which    therefore 


comprises   a 


11   th 


processes 


which  are  held  to  lie  comj ')n(>nt  parts  of  an  inflanunation,  should 
hav(>  added  to  it,  when  necessary.  (lescrii»tive  terms,  not  definiiiff 
particularly  the  location  of  the  infl.anunation  or  its  patho<i-enesis. 
hut  purely  descriptive  of  the  predomin.-itin-i-  patholojiical  feature 
or  features.  In  this  regard  the  classilication  of  Delafield"" 
a  considerahle  forward  step. 


was 


•2.  In  certain  forms  of  nephritis,  when  predoniinatinji  features 
are  lackin<>  or  of  minor  importance,  no  such  tlescriptive  terms  are 
reijuired.  These  I  jiioup  as  nephritis  simplex.  This  type  is 
represented  mainly  hy  varyinji  comhinalions  of  parenchymatous 
deo-onerations  and  ii.flammatorv  (edem;i. 


HISTOHK  AI.    INTKODl  CTION    AM)   (I.ASSIFICATIO.N 


3.  Whon  cortain  iiiflaiiunatoiy  attril)Ut('s  predominate,  thcv 
are  added  as  (lualifications  to  the  term  nephritis.  In  this  sens(> 
I  speak  of  nephritis  defienerativa.  exiuhitiva,  luemorrha<;ica,  and 
proHfera.  It  may  he  one  or  more  that  are  mark»'d  in  this  way. 
To  sijinify  any  particularly  i)roniinent  location,  one  can  adil 
tuhularis  or  jilonieruhiris. 

4.  When  in  certain  kidneys  fatty  chaiiftes  occur  which  assume 
<ireat  prominence,  the  lesion  is  spoken  of  as  nephritis  de<ienera- 
tiva  adiposa. 

.').  \\hen,  in  such  kidneys,  loss  of  parenchyma  occurs  with 
connective-tissue  jjrowth  and  vase  Jar  chanftes,  the  term  nephri- 
tis dcfrenerativa  et  productiva  is  employed. 

().  When  the  loss  of  kidney  substance  is  extrer  ■.  with  a  thick, 
fil)rous.  connective-tissue  <j;rowth.  marked  vascular  chan<ies,  and 
the  (le<;enerative  chan<;es  not  prominent,  we  may  speak  of 
nephritis  productiva.* 

7.  Finally,  there  exi.sts  an  atrophy  of  parenchyma,  either 
ah)ne  or  with  marked  arteriosclerosis  and  patchy  fibrous-tissue 
firowth,  typified  in  the  senile  kidney,  and,  as  I  l)elieve,  really  not 
of  an  inflannnatory  character.  This  is  termed  atrophia  and 
sclerosis  renum  respectively.  I  include  it  here  for  the  .sake  of 
discussion. 

Xo  doubt  combinations  of  these  forms  and  types,  which  we 
can  recojinize  only  in  a  wider  sen.se,  are  frecjuent,  and  should  then 
l)e  named  and  da.ssified  accordinjily.  This  point  will  appear 
more  fully  in  a  detailed  di.scussion  later. 

I  trust  you  have  followed  me  sufficiently  to  appreciate  the 
desirabil'ty  of  a  break  with  the  older,  current  classifications,  and 
to  sul)stitute  a  simple  descriptive  terminolofty.  I  believe  fully 
that  only  on  the  basis  of  clearer  anatomical  pictures,  which  this 

*  Till'  Icrtii  prixliiclivo  niiiy  st>cm  objectionaWo  to  some.  a.s  thpformiition  of  nrw  tissue 
concerns  largely  the  supporting  .structure,  hut  it  i.s  perliaps  admi!<sil>lo  wlicn  it  is  considered 
that  far-reuchiiig  inoditicatiua  of  cells  occurs  in  the  essential  parenchyma. 


1  , 


'm 


26 


HHKiHTS    DISKASK 


iioimMicl.'itiirc  aims  at.  will  1  tetter  knowledjie  iie  diseases  of 
tlie  kidiiev  he  made  |)<>ssil)le.  not  only  for  tli  uiids  of  the  in- 
vest iiiators.  wlio  larucl.v  do  not  understand  each  other  now  and 
l)attle  with  words,  l)Ut  particularly  for  those  diaftnosing  and 
treatin"  them. 


Sl-X'OXI)  LIXTIHi:* 
Thk  STurcrrHK  ok  thk  Xohaiai,  Kidnky  and  thk  Difkkkkxt 

\'lK\VS   ON    ITS    Fl  NCTIONS    IN   THKIK    HkI.ATION    TO   THK 

Pathoi.<)(;i('ai.  \'ahiatio\s 

(icntlcincn: 

H(>f()r('  \\v  cutor  uj)()n  our  suhjoct,  I  tliink  it  wise  to  recall 
to  your  niiud  cortain  histolo<>ical  and  physiolojiical  facts  and 
theories.  Unfortunately,  they  are  not  as  complete  as  we  would 
like  to  have;  particularly  on  the  physiolo<>ical  side  testimony  is 
scant.  The  role  played  in  the  .secretion  of  the  urine  hv  the  vari- 
ous component  parts  of  the  kidney  is  not  definitely  .settled;  and 
if  this  knowledfic  is  deficient  on  the  physiolof^ical  side,  we  are  in  a 
jM'rfect  chaos  of  conflictin<>:  testimony  on  the  patholo<iical  side, 
into  which  we  can  l)rin<i  lij;ht  and  reason  only  with  much  diffi- 
cu!t>-.  We  may  admit  from  the  start  that  there  is  really  not  one 
theory  of  urinaiy  .secretion  which  directly  conforms  with  all  the 
patholofiical  evidence,  and  allows  us  to  form  clear  conceptions  of 
the  patholojiical  variations.  The  reason  for  this  will  appear 
later.     Let  us  examine  what  evidence  there  is.' 

Commencinff  with  histological  considerations,  I  believe  I  may 
disregard  in  these  lectures  the  emhrvolofiv,  and  immediately 
invite  your  attention,  with  the  aid  of  this  diagram,  to  the 
structures  of  the  normal  adult  kidney  ( Plate  1 ).  You  know  that 
it  is  composed  of  two  easily  recognizable  and  separable  parts; 
The  outer,  or  corte.x,  and  the  inner,  or  medulla,  which  stands  in 
direct  communication  with  the  pelvis.  Both  of  these  enter, 
however,  upon  the  field  of  the  other,  for,  as  you  see,  the  medulla, 

•  Delivered  on  Janiuiry  21,  1909. 


■js 


HUKillT  S    DISKASK 


l)y  cliMnictciislic  r;i(li;itiiiir  lines,  sciuls  ot'fspriiiiis  into  the  cortex, 
known  .is  in(>(hill;irv  r;iys:  while  in.isses  of  cortex  se|);ir;ite  parts 
of  tile  niednila.  tlie  pyramids,  liy  tlie  so-called  colunuisof  Hertini. 
The  inedull.iry  r.iys  .are  produced  hy  a  rejiular  inierclianjie  (»f 
ves.sels  with  the  collectinu  and  str.iiiiht  tuhiiles.  the  .ascending 
and  desceiidini:  loops  of  Henle.  'I'he  cortex  proper,  on  the  other 
h.and,  contains  the  iiloinenili  and  the  proximal  .and  dist.al  ends  of 
the  convoluted  tul)iil(>s.  |{eferrin<i'  to  the  dia;;ram,  you  appre- 
ciate the  lonji  a!id  p.irtly  tortuous  course  of  one  of  these  units, 
connnenciiiii  with  the  cortical  jrlomerulus.  and,  after  a  lonji. 
v.aried  route,  endinji  in  the  pelvis  of  the  ki(hiey.  Particular 
attention  should  l)e  paid  to  the  ditTerent  calil)er  of  the  tubules  in 
different  p.irts,  and  the  very  abrupt  chaufie  from  the  broad, 
ctMivoluled  tubule  to  that  of  the  strai<-ht,  narrow  liml)  of  Henle, 
with  the  interpolation  of  a  second,  but  nuich  shorter,  convoluted 
portion,  which  finally  empties  into  the  collectinj;-  tubules. 

I  think  it  proper  to  briefly  describe  the  m.ain  features  of  the 
blood-supply  iiefore  speaking-  of  their  finer  structure. 

It  is  very  suiijicstive.  All  conditions  are  jiiven  whereby  a 
laruc  amount  of  Itlood.  under  a  very  hiuh  pressure,  can  be  brought 
to  the  kidney  (lir(>ctly.  without  passinji  throuiih  many  divertinji 
channel:  The  reii.d  artery  is  a  rather  short,  thick  brancli.iiiven 
off  directly  from  the  aorta.  It  proceeds  to  the  hilus  of  tlie 
kidney,  where  it  immediately  divides  into  .several  branches  which 
ascend   to  the  point   of  junction   between   the  cortex  atid   the 


medulla.     The  first  liranch  of  the  renal  art 


cry  is  s|)oken  of  as  tli 


interlobar  artery,  while  its  branches,  which  you  see  represtMited, 
are  spoken  of  as  the  interlobular  arteries.  They  proceed 
up  throu-ih  the  cortex  and  down  throu-ih  the  medulla.  In  the 
cortex  they  pass  directly  to  the  domerulus. 


The  formation  of  a  jilomerulu 


s  is  intere.stiii<;.     It  i.s  a  lobular 


structure,  c(>mi)osed  of  a  vascular  network,  kn 


own  as  capillary 


STUrcTlUK    AM)    FIXCTIONS    OK    THK    NOIf.MAI.    KIDXKY        29 

tuft,  ami  enclosed  in  what  is  ternicd  Howinan's  capsulf.  It  is, 
luoicovcr.  peculiar  and  characteristic  that  the  afferent  vessel  of 
the  jilonieriilus  is  very  much  lar<;er  than  the  efferent  or  centri- 
fuj-al  vessel.  In  other  words,  the  hlood  is  hrouj-ht  under  hiiih, 
almost  direct,  aortic  pressure  to  the  <ilomerulus,  hut  in  the  filo- 
merulus  it  is  under  still  hijiher  pressure  am',  distrihuted  over  a 
relafivly  lar-ic  surface.  So  much  is  plain  from  anatonucal 
ol  nervation. 

Havin-i-  left  the  jilomerulus,  the  vas  efferens  immediately 
l>reaks  up  into  a  capillary  network,  and  this  network  follows  the 
convoluted  tubules.  Hefore  the  hlood  reaches  the  convoluted 
tuhules  at  all.  it  must  <i;o  throujrh  a  <ilomerulus,  and  the  hhxul 
which  jioes  to  the  tuhules  is  under  a  relatively  lower  pressure, 
compared  with  what  prevails  in  the  ^lom(>rulus  and,  as  will 
;il)pear  later,  must  have  a  jireater  concentration.  The  veins 
which  correspond  to  the.se  arteries  are  es.sentially  the  .same, 
with  the  only  exception  that  they  do  not  enter  the  jilomer- 
ulus. 

The  lymphatic  vos.sels  of  the  kidney  are  not  very  well  known. 
It  is  supposed  that  tliey  accompany  the  vessels.  It  is  douhtful 
if  there  ;ire  any  in  the  filomerulus. 

With  regard  to  nerves,  there  exists  a  complex  derived  from 
the  renal  plexus  and  le.sser  .splanchnic.  They  accompany  the 
ves.sels  and  :dso  extet.u  to  <i;lomenili  and,  as  some  suj)po.se,  to 
the  epithelium  of  the  convoluted  tuhules.  This  latter  point 
is  uncertain,  and  the  presence  of  .secretory-  nerves  has  never 
l)een  conclusively  demonstrated.  Nervous  influence  may  he 
explained  on  the  hasis  of  vasomotor  action. 

\\e  come  now  to  the  important  consideration  of  the  structures 
of  the  es,sential  parts  of  the  kidney.  The  <tlometuli  and  the 
tuhules  are  lined  throujrhout  hy  epithelium,  hut  it  is  different 
epithelium  in  different  parts.     In  the  glomerulus,  it  is  made  up 


1|  I 

p 

li 


r 


:{() 


HI'*(;HTS    DISKASK 


of  two  l;iycrs.  I  ipitlicliuiii  lilies  tlic  ciipsnlc  ;iii(l  is  reflected  over 
llie  tuft,  liut  (inly  su  ns  to  p;irtly  (-((ver  this.  It  is  stated  hy 
lleiiiiiii  '  tliiit  I  he  e|)it  helium  of  the  cMpsule  is  of  ;i  lower,  more 
endolheli.il,  syncytial  t\  |H',  while  the  reflected  epithelium  of  'he 
tuft  is  of  ;i  ure.iter  ditTercntiatioii.  ;iiid  res(>mltles  somewhat  (he 
secretory  epithelium.  .\t  the  point  of  entrance  of  the  first 
convoluted  tiiimle  the  epithelium  ch.an^ics  <:radually.  so  that 
tr.-insitioii  cannot  lie  definitely  estalilishe<l  at  any  particular 
|>iiiiil. 

The  epithelium  of  the  convoluted  tuliules  is  hijili.  well 
difTerenti.ited.  The  iiiich  us  is  situated  near  the  tunica  propria. 
'Ihe  protoplasm  is  extremely  jiianular.  These  ^taiiulations  are 
arranged  in  definite  order  of  streaks  or  rods.  Their  extremities 
are  delicately  liruslied  with  non-motile  cilia. 

'ihe  epithelium  of  the  descendinji  limh  of  Henle  is  low  and 
Hat.  it  is  rather  poorly  defined,  so  that  the  line  of  demarcation 
between  the  different  cells  is  not  clear,  and  it  looks  more  like  a 
.syncyti.il  formation  or  the  e|)itlielium  of  the  cai)sule  of  the 
•glomerulus. 

The  epithelium  of  the  a.scendinji-  limh  of  Henle,  as  well  as  of 
the  distal  end  of  the  convoluted  tuhules.  is  hi<iher,  and  a<>ain  he- 
eomes  distinctly  <>;ranular.  somewhat  re.semhliiifj  the  epithelium 
found  in  the  proximal  limb  of  the  convoluted  tubules.  This  is 
<riv(Mi  by  .some  as  cylindrical  epithelium,  a  doubtful  statement 
for  the  normal  human  kidney. 

The  epithelium  of  the  collectinj-  tubules,  finally,  is  hijrh,  clear, 
and  not  jrraiuilar,  while  the  lumen  of  the  tubuleitself  is  very  larfre. 
You  can  see.  therefore,  that  there  are  e.ssential  differences  in  tlie 
make-up  of  these  important  structures.  We  are  unable,  how- 
ever, to  correlate  with  the  same  ease  the  functional  differences. 
Wo  have  evidence  which  brings  in  a  <reneral  way  the  epithelium 
of    these  various  part.s  in  relation  to  certain  functions;   but  no 


STIJI  (TlUK    AM)    Kl  MTKINS    OK    THK    NnllMAI.    KIDNKV        ,'il 

;il>s(.lut('  proof  exists  ;is  rcjr.-iids  their  spccinlizcd  duties. 
I'ossil.le  excepti(»ns  :ire  only  tlie  ;ilom(>niliis  mikI  the  proxi-  il 
eoiivoluted  Hil)ule,  ;il)oiit  whose  (hities  we  are  somewhiit  Ix'tter 


iiiforined  th:in  al»out  the  rest  of  the  stnieture. 

So  iiiiich.  then,  for  anatomical  considerations.      Tl 


ic  arrantre- 


nient  ditTiTs  from  that  (tf  other  glands  mainly  in  tlu'  hlood- 
supply  and  in  the  peculiar  course  and  structure  of  the 
secret  in;;'  surface. 

I  must  now  review  the  various  conceptions  which  are  held 
with  re^Mrd  to  the  .secretion  of  urine.'     The  (»ld  idea  had  heen 


that    the   kidiiev   wa? 


es.sentially  a   filter,   that   is,  a  structure 
lU'inarv  constituents 


throu;ih  which  water  and  the  characteri.stic 
were  pas.sed  hy  a  simple  process  of  filtration.  That  idea  gained 
ground  particularly  after  Bowman's  classical  description  of  the 
^domerulus.  Hut,  on  account  of  the  length  and  the  es.sential 
structural  variations  of  the  tuhules,  it  soon  appeared  that  a 
specific,  secr(>tory  function  on  their  parts  was  also  prohahh'. 
Thus  Bowman  (1S42)  '  himself  l«>lieved  that  the  ^domenilus 
filtered  water,  i)Ut  that  the  tul)es  were  a  secretorv  structure,  and 
he  based  his  ideas  entirely  on  the  previously  detailed  anatomical 
considerations. 

Ludwi^S  who  in  1S44  puhli.shed  his  cla.ssical  observations,  at 
the  time  of  strongest  conflict  between  vitalists  and  mechanists, 
wa-  I  he  first  to  offer  a  purely  physical  theory.'  In  substance, 
this  theorv-  assumes  that  all  urinar>'  constituents  transude 
throu^di  the  ^domerulus,  uiuler  the  force  of  its  hi^h  pressure  and 
in  v(My  dilute  .solution.  Passing'  through  the  tubules  a  re-sorj)- 
ti(m  of  this  water  to  the  more  concentrated  lymph  occurs;  the 
fluid,  therefore,  assumes  its  urinous  character. 

Ludwi^-  based  his  ideas  of  filtration  on  the  fact  that  the 
amount  of  urine  depends  mainly  on  the  arterial  pressure  and  on 
the  rapidity  of  flow  in  the  kidneys.     If  the  arterial  pressure  is 


i 


m 
I 


32 


HIIKIMT  s   l>lsi;\sK 


iiiciVMSfd.  Mini  if  llic  rMl«>  <>f  flow  of  the  M 1  lliroii<ili  the  ki(lin>y 

is  also  iiK  ivasrd,  tlicii.  of  coins.',  llif  aiiioimt  of  uriiif  iiicivascs. 
If.  on  the  oIIht  liaiiil.  wc  li.ivr  .1  diiniimlioii  of  llir  aiit-rial  lucs- 
siiiv  ill  the  kidiK'v.  .iiid  a  diiniinilioii  of  llir  rate  of  flow  <>f  the 
l.lood  tliroiiiili  llir  kiiliK-y.  tlioii  the  amount  of  urine  decreases. 
Tliis  is  a  perfecllyol'vioiis  fact.. and  is  also  suppoited  liy  patho- 
logical e\idence>.  We  know  that  in  eases  of  inccmiplete  coin- 
pensati<in  of  the  heart  the  amonni  of  urine  diminishes  markedly. 
It  is  als<i  cert.iin  that  when  the  reii.al  artery  is  obliterated,  the 
same  holds  true;  and  when  the  arteii.al  pressure  in  the  kidney 
is  in.irkedly  diminished.  ,as  in  section  of  the  spinal  cord,  there  is 
M  consideial'le  diminution  in  the  volume  of  mine.  On  the 
other  hand,  division  of  the  renal  nerves  produces  va.soiiKXor 
pai;iI>sison  that  side  and  the  urine  is  increased.  Stimulation  of 
the  spinal  cord  and  the  splaiichnics  raises  the  Mood-pressure, 
and  h:is.  therefore,  the  same  result. 

Further  corrol>oration  is  found  in  the  dose  relation  of  the 
amount  of  fluid  taken  to  that  excreted,  so  that  the  (juantity  of 
urine  de|)ends  laijidy  upon  the  pro|)ortion  of  water  i)resent  in  the 
lilood.  If  a  person  drinks  laiiic  amounts,  there  is  an  i.lino.st 
immediate  response  on  the  part  of  the  kidneys.  The  effects  of 
cert.iin  driiiis.  like  cafTein  and  diuretin.  have  also  been  looked 
upon  as  favorable  to  this  idea,  in.ismucli  as  ;heir  action  is  con- 
sidered to  depend  upon  .an  increas(>  of  blood-current  due  to  a 
vascular  dil.at.ation.  .althoiiiih  this  has  been  disputed. 

Now.  in  order  to  explain  certain  properties  of  urine,  which 
caimot  be  accounted  for  by  the  <lirect  application  of  simple 
filtration.  Ludwiy.  resorted  to  another  theoretical  consideration, 
which,  in  his  opinion,  explains  the  complicale(l  and  perplexinji 
structure  of  the  tubules.  He  held  that,  while  a  transudation 
occurs  in  the  glomeruli,  re.sorption  of  water  occurs  in  the  down- 


STin  (Tt  IIK    AM)    Kl  \(  TIONS   «»K   tiik    .\, 


m.MAr.    KIDNKV       IV.i 


Ward  flow.     'I'liis  !irc<tiiiits  for  the  rcl.-it 
riiK'.   which   is  iinich  ;irc:il(i-  tluin   that   of  the  Mood,     h,  | 


ivc  coriccnt radon  of  ih«' 


u 


ll.S 


••pinion,  thcicfoir.  tlic  tul.nlcs  exist   mainly  for  the  pr(Mrs.s  of 
water  resorption. 

It    must    he  (-(.nfe.ssed  at   oiwe   that    there  is   no  ahsoliitelv 
••onclusive  proof  of  wat«'r  res<.rption  hy  the  tiilniles.     'M 
periments  of  IJibhert  on  the  ii 


le  ex- 


icreased  flow  of  urine  water  aft 


the  resection  of  the  medulla  have  U-en  contra<licted  l.y  lioy<|, 
iMit  lat'.r  evidence  alonj:  this  line  has  hec  n  |)articularlv  offered 


nd  upheld  liy  Cushnv  and  Hans  .M 


ever. 


Ii 


owever.  there  is  also 


much  ajramst  it, 


I'or.  inasmuch  as  the  urine  has  a  hi<d 


ler  osmotic  pressure  than 
the  Mood,  it  follows  that  a  simple  resorption  seems  to  he  out  of 
<|Ue.stion,  hut  we  must  assume  for  this  active  work  on  part  of  the 


epithelial    cells   of   the    tul)ules.      It    has   I 


Dreser"  that,  in  order  to  (>fTect  tl 


K'en   fi^iured   out    h 


lis  concentration,  if  would  re- 


<|uire,  under  circumstances,  a  force  .six  t 


imesjtreater  than  that  of 


human  muscle  (,S(MK)  jjm.  per  .s(|uare  centimeter),  die  deprived 
a  cat  of  water  for  three  days,  :ind  then  drew  olT  the  urine,  which 
had  a   freezin«t-point  of 


4.72°  (*.     The  hlood  at  tl 


le  .san>e 


time 


Had 


().()()°  C.  Now  von  fHofT  ha.s  shown,  if  is 
the  dei)re.ssion  of  the  frcezinji-point,  and  T  the  ah.solute  freezin<r- 
point  of  the  solvent  (for  H,()  27;i°  and  w  the  latent  heat  of 
fusion  of  i<'e 
this  fornmla 


7!)  cal.i.  then  the  work  A  can  I 


)e  reckoned  from 


(lA  =    ^    X  (Iv. 


Thus  for  1  per  cent,  solution  of  cane-sufi! 


tr  (  O.Ooo): 


,.       0.0-).-).  7!» 
<IA  =      .,..,      X  (Iv. 


To  reduce  this  result  to  <rravitation  units,  we  must  multiplv 


:m 


l.v    l_M.  :'ii( 


Hifniiiis  i»ink\-k 


1  thus  liii.l  lliMl   «>  s«'|.:il!itc  llic  volumr  tlv  of  |)un' 


\v:i 


trr:isi.Tfr..m  1  |mt  <riil .  cmiu'-siii;:.!- so 


lulitiii.  ;i  force  is  lu'crs- 


siirv  ctniM 


1  tn  llic  picssilivitf  M  roliilllli  of  W.ilcio 


(».().'».')  X   I 


lUflcrs    III 


liciiilit.       A    (Icprrssiofi    o 


f 


ihcrcfoiT.  to  Mil  osmotic  pressure  o 


»•_'» 


«.»      424 

\'^   correspoiKls, 
tliiil    is  to   s:iy. 


to  IJJ.T  liielei>  of  water. 


I  •_*•_'. 7  in  or 


We  li.ive.  tlierefore,  to  uiiilliplv       l> 


,1,.,.  ,„  ,,l.t:iiii  the  osmotic  pressure  in  metefs  of  water 


in  Miiv  solution. 


In  tl 


le  ciise  o 


f  the  c:il  just  mentioned.  thes<>  differences  in  the 


freezin^-jMiinl  denote  an  «»sino 


tic  (HtTerence  of  JUS  meters  water. 


f  l*.».S(M»  i:m.  iH'r  s(|uare  centimeter 


/.  ( ..  a  pressure  o 

Dreser  has  eiideavoret 
"ilomeruli.  to  demon: 
the  liniiiy:  epillielial  cell^ 

I'rom  our  standpoint   there  are,  a^ 
pointed  out,  son 


>f  I 


11(1  win. 


1  to  silow  the  same  with  rejrard  1o  the 
itratj-  in  tliem  al.so  active  work  on  l)art  of 

MiiUer"'  has  only  lately 

Itjections  to  accept  the  |»ure  filtration  idea 

We  all  know  that  in  chronic  venous  con^jestion  the 


le  o 


iiinoi 


ml    of  urine   is  niK 


h   diminished,   while   tin*   secretion   of 


mtroiienoi 


IS  material  is  kept  up  to 


Ilea 


in  extreme  ca 


ses  of  oliiruria.     Mow  can 


rly  normal  limits,  except 
i.udwiji  then  account  for 
this?  One  would  li.ive  to  suppose  an  almost  normal  transuda- 
tion from  the  ;rlomeruli  with  an  inrmis,<l  resorption  from  the 
tuhuh's.  That  seems  unreasonal>le  from  phy.siolojiical  and  tele- 
olofii.-al  considerations,  for  an  injured  kidney  would  Ik>  called 
\ipon  to  do  more  W( 


irk,  to  the  iiijur>-  of  the  patient. 


For  similar  reasons, 


Midler  holds  an  explaiiatum  of  the  hir<ie 


amount  of  urine  in  dial)etes  insipidus  diHicult,  and  the  same 
applies  to  the  increase  in  urine  in  certain 


form^' 


of  pure  produ 


tive    (interstitial)    nephritis. 


ihere    evidence    showed    irn  iter 


iffection  ( 


if  the  tubule; 


if  the  domenili  and  less  involvement  of  the  ('|)ithelium 


STHI  I  Tl   UK    AM)    Kl   V<TIU\s   ilK    TM  K    NOli.M  \l.    KII)NK\         'MS 

I  will  point  out  hilcr.  liowi  r.  lli.il  we  iiiiist  !»«•  vfrv  careful 
to  (lirt'ctly  apply  patlmlojiical  fimi-tioiis  for  tlw  pr»M»f  or  disproof 
of  plivsioloiiical  coiitciitioiis.  as  we  liav«'  fr«'(|Ufiilly  cnlin'ly 
(lilTcn'tit  anatomical  coiulitioiis  ami  rcarraii^cmciits  of  the 
parts.  1  liflicvc  Ludwi-i's  theory  particularly  weak  in  its  lack 
of  cojiiii/.aiicc  of  certain  inetaholic  finictions  on  tin'  part  of  the 
kiilnev.  Iiesides  the  elimination  of  urine.     We  kn<t\v  that  certain 


■lynthetic  prt)cesses  a 


re  actively  carried  on  in  th<'  kidney.     The 


ormation  o 


f  hipi 


)nnc  act*! 


fr< 


om  <;i\('oco 


II 


in< 


I    U'lizoic  aci<i  is 


perhaps  Itest  known  aiitl  studied:  yet  there  are  und(»ul>tedly 
others,  like  the  formation  of  the  urinary  chromoj-cns.  <'tc.  There 
can  lie  no  quest  ion  that  the  epithelium  of  the  tulmles  of  course, 
we  do  iKtt  know  which  imist  lie  actively  concerned  in  this 
formation,  and  that  these  substances  are,  in  all  pndtahility,  di.s- 
chaified  directly  into  the  tuhules.  It  certainly  ap|M'ars  that,  if 
a,  all.  a  resorption  of  water  camiot  Ih-  the  sole  duty  of  the  tiihules. 
'I'hese  ideas  of  Ludwiji  h;ive,  therefore.  I leen  actively  and  Imt- 
manentlv  op|)osed,  primarily  l)y  lleidenhain  and  his  followers. 
Ileidenh.ain  "  took  the  extreme  other  view,  attrihutinjr  the  whole 
process  to  ;in  active  secretion,  and  denyiiifi  any  iiltratioi\.  His 
ideas  were  essentially  based  on  three  i)oints:  If  one  ties  the  renal 
vein,  the  intrafrlomerular  pressure  is  increased.  In  spite  of  that, 
the  urine  is  not  increa.s<'d.  hut  diminished.     If  one  ties  the  renal 

Uately 
II 


lese 


arterv  and  then  relea.ses  it.  the  flow  of  urine  is  not  iiiime( 
recstal)lishe(l.  imt  only  .after  a  consideral)le  time, 
phenomena,  he  arirues.  speak  ajiainst  a  simple  transud;;tive 
character  of  urine  water.  Hut  the  fact  to  which  most  im|K)rtanee 
is  attacheil  is  the  result  of  experiments  after  the  injection  of 
indijio  caniiin.  He  found  that,  if  indijio  caiinin  was  injected  into 
the  renal  artery  and  the  animal  was  killed  after  ten  minutes,  the 
indiiro  carniin  was  always  precipitated  in  the  epithelium  of  the 


convoluted  tuhules.    It  was  never  found  anywhere  else. 


I'rom 


nuKiin's  nisKASK 


that  he  coiicludod  :i  siM'cific  select 


ivc  ;n 


■tivitv  oil  the  part  of  that 


portion  of  th(>  reiia 


Icpitlicliinii. 


Now.  all  <)f  these  three  arjiimiei 


Its  of  Heideiihain  have  not 


stoot 


1  the  test  of  time  uiKlispiited.'"      'I'he  resi 


ilts  of  tviiiii  the 


r(M\ 


,1   vein  and   tliiis    iiicreasiii-j 


mav  eas 


without  increase  ot  iiniu 
stasis.  .\  diminution  in 
to  purely  mechanical  causes,  nanu 


the    intra-jilomerular  pressure 
ilv  he  attributed  to   venous 


the  amount  of  urine  may  there  he  (hie 
■ly.  pressure  of  the  prrts  fjiainst 


another,  a  resu 


lit  of  the  venous  enjiorfi(  meiit . 


Similarly,  the  secoiK 


1  ariiument.  tvinii  the  renal  artery,  with 


out.  o 


II  its  release,  ohtainin-:  an  unmet 


Hate  How  of  urine,  appoan 


of  (loul)tful  va 

kidnev.  it  would  take  consii 

and  rapidity  of  flow  ar(>  rei 

Kinallv.  the  most  impcu 


hie.  because,  in  a  comi)li("ite«l  strueturf 


like  th 


the  results  o 

denied  its  value  by  many  mvestiji 


lerable  time  before  normal  pressure 

■stablished  in  the  -ilomeruli. 

■tant  arjiument  which  he  advanced. 

iniin.  has  been 

;ti"ators  who  claim  that,  if  the 


)btaincd  from  injection  of  indi'io  c:i 


no 


solution  of   indiiro  carmin    b 
Heidenhain  employed,  and  if  the  kidnr 


t    of   the   exact    concentration 
•v  is  examined  earlv  after 


injection,  thi 


bstance  is  a 


Iso  found  in  the  liiomeruli.  so  that 


111  rea 


,litv  sele.-tive  activity  docs  not  occur.     It  has  further  becMi 


pointed  out  that  on  its  wa> 


a  <ioo( 


I  deal  of  the  pifiUient  mi; 


ht 


UIK 


ler'o  a  reduction,  w 


herebv  it  would  not  be  visible  in  other 


(•( 


■Ih 


(IK 


1.  hiiallv,  much  of  the  indigo  carmm 


in  the  epithelial 


cells  of  the  convo 


ihited  tubules  is  nearer  the  lumen 


)f  the  tubule 


so  'hat  one  n 


li-dit  ar"ue  that  it  were  o 


II  its  wav  from  the  lumen 


to  thel)lood.  and  not  vice  versa. 


This,  of  course,  would  conform 


with  Ludwi;:  s 


view: 


that  these  id(  as  of  Heidenhain,  altliou^ih  accejMed  b 


m 


You  see 
anv,  stand  on  :i  very  < 


lisputed  experimental  basis. 


("•.rave  patliolojiical  evi<lenc(>  has  also  been  brou-ht  forward 


a>!;ai!ist  the  sweepin^i  secret 


orv  ideas  o 


if  Heidenhain  bv  Senator. 


i*i 


STIUCTIKK    AM)    KINCTIONS   OK   THK    NOKMAI.    KIDNKY        37 

\V(>  know  a  nunilxM-  of  kidney  lesions  tissociated  with  extensive. 
Mlthoujrh  slowly  projiressinji.  destruction  of  the  epithelium. 
Accept iiifi  nei.ienhain's  views  of  a  purely  secretory  function  of 
the  epithelium,  one  should  reastmably  expect  a  jrradual  diminu- 
tion in  the  amou.it  of  urine  in  these  lesions.     But  the  facts  speak 

differently. 

Path()l()jrists  and  clinicians  have  known  for  a  lonji  time  that 
in  certain  types  of  productive  nephritis,  and  in  the  amyloid 
kidnev,  the  amount  of  urine,  instead  of  heinji  diminished,  is 
a.-tuailv  markedly  increased.  The  gradual  loss  of  epithelium  of 
jrlonieruli  and  tubules  does  not  seem  to  have  the  slightest  relation 
U)  the  urine  output .  How.  asks  Senator,  can  this  \w  rejiarded  as 
the  active  product  of  the  e[)ithelium? 

S(Miator,  in  conjunction  with  Munk,  bejjan,  therefore,  ♦o  in- 
vest i^^ate  that  [)oint  further."     They  were  aided  by  a  discoverj-, 
made  shortly  before  by  Hoy  and  others,  namely,  that  it  is  possible 
to  have  kidneys  functiotiate  after  they  have  l)een  removed  from 
the  body.     Takinj:  advantafje  of  this  method,  they  transfused 
defil)rinate(l  blood  through  kidneys,  and  were  able  to  observe 
closely  the  results  of  chan<rin}i  pressure  and  rapidity  of  flow 
l)roujiht  about  artificially  in  transfusion.     They  found  the  fol- 
lowing: facts:    In  active  hyix-nemia-in  other  words,  when  the 
pressure  as  well  as  the  velocity  of  the  flow  is  increased— the 
rjuaiitity  of  urine  excreted  increases.     The  quantity  of  nitrojien 
increases,  while  that  of  the  sodium  chlorid  shows  ver>'  little  va- 
riation from  the  normal.     That  latter  point  is  interesting;  and 
important  to  remember. 

Then  they  did  the  opposite,  diminishinj:  the  quantity  and  the 
pressure  throu«:h  the  kidney,  with  these  results,  that  the  amount 
of  vnitie  decreased  decidedly,  that  the  amount  of  nitrofjenous 
material  also  decreased  decidedly,  while  the  amount  of  sodium 
chlorid  showed  no  difference  from  the  normal.     Incidentally,  I 


i 


:{s 


HKKIIIT  S    DISKASK 


should  mention   tli:it    tlic  :iniount   of  ;ill)iiinin  wliid'     ucli  an 
artiticial  urine  al\va\  s  shows  diniinished  with  arterial  hypera-niia, 


am 


en 


1  increased  with  passive  hypera 


tnia.  Interestinji  is  the  ex- 
■tion  of  sodium  chlorid.  which  remained  practically  imaffected 
l)y  active  hypera-mia  or  stasis.  It  arsiues  for  an  at  least  partly 
traiisudative  character  of  the  urine,  for  pressure  and  rapidity  of 
a  transudiiiii  fluid  determine  the  (plant ity  of  a  transudate,  hut 
not  its  amount  of  dis.-^olved  cry.-^talline  substances. 

Based  on  these  considerations,  they  concluded  that  the  lu-ine 
must  he  regarded  jjartly  as  a  transudation  and  partly  as  a 
secretion.  The  transu(lativ(>  part  is  furnished  hy  the  jilomeruli, 
the  arraiiitement  of  which  is  also  very  nuich  in  favor  of  its  l)ein<r 
a  transudin<r  memhrane.  This,  however,  has  added  to  it  on  its 
way  throuirh  the  tul)ul(>s  a  secr(>tion  of  the  epithelium,  which  is 
also  in  watery  .■solution.  The  combined  fluid  is  taken  up  by  the 
collectinii  tubules  and  discharired  into  the  pelvis  of  the  kidney 
as  urine. 

These  ideas  also  have  underjione  revision  by  other  investi- 
•rators.  It  has  been  urjred  that  it  really  has  not  been  demon- 
strated beyond  doubt  that  the  jilomeruli  filter  only  water  and 
sodium  chlorid,  and  as  a  contradictory  fact  is  mentioned  that  in 
arjivria  the  silver  imprejiiiates  the  loops  of  the  jilomerular  tuft. 
It  is,  therefore,  argued  that  these  tufts  ar(>  probably  permeable 
for  other,  normal,  urinary  substances.  Aiiain,  it  has  l)een 
claimed  that,  if  the  jilomeruli  truly  filtered,  sujiar  as  well  as  albu- 
min ouiiht  to  be  found  in  normal  urine." 

.\11  of  these  oltjections,  howev<'r.  carry  very  little  weijrht. 
That  a  foreign  subst.iiice  like  silver  is  arrested  in  the  <ilomerular 
tuft,  which,  on  account  of  its  arran^rement,  seems  to  be  particu- 
larly exposed  to  the  acc\unulation  of  foreign  material  withifi  its 
loops,  camiot.  in  my  opinion,  carry  imich  evidence  as  regards 
normal  functions.      The  other  two  objections  have  lost  much 


STUrCTl  UK    AM)    KlNiTIONS    OK    THK    N<tHM.\l.    KIDNKY 


39 


jrrouixl  siiKT  it  has  l.o.-onu'  -ejiorally  known  that  varyinj:  traces 
of  all.uiiiin  occur  in  all  urines,  and  that  su-ar  circulates  in  colloid 
form.  Hans  >hner  believes,  therefore,  that  the  filonieruli  Hlter 
all  the  sul)stances  which  are  contained  in  the  blood  in  cr>s{alline 
form,  while  the  convoluted  tubules  secrete  such  substances  as 
are  in  colloid  state  (urea.  uric  a.-id.  phosphoric  acidi.  He  and 
other  investigators  have  revived  for  this  latter  i)rocess  Ludwi-'s 
idea  of  water  and  Na("l  resorption. 

Hans  Nh'ver.  Cushny.  and  Hausmann  found,  as  previously 
mentioned.'"'  after  extirpation  of  the  medulla,  an  increase  of  from 
th-e  to  four  times  in  urine  quantity  with  a  proportionate  de- 
crease in  concentration.  Meyer  states  that  •'  the  excretion  of  ("1 
and  X  after  such  operation  corresponded  to  the  contents  of  the 
l)lood.  so  that  the  fluid  eijualed  an  albumin-free  l)lood  Hltrate.'" 

Hans  Meyer.  I/.wi.'"  (lottlieb.  Mafimis.'^  an<l  Cushny  also 
fovnul  that  after  injection  of  sodium  sulphate  ((llaubersalz) 
into  the  blood,  a  much  more  active  diuresis  occurred  than  after 
injection  of  a  corresponding  amount  of  sodium  chlorid.  Meyer 
conchuled.  therefore,  that  this  acted  similarly  in  the  kitlney  as 
in  the  jrut.  prevented  resorption,  and  cavised,  so  to  siH-ak,  a 
renal  diarrhea.  It  has  also  been  shown  by  Cushny.  Pfaundler,'^ 
and  Steyrer'"  that  resistance  in  the  ureters  is  associated  with  the 
's.>cretio"n  of  a  verv  thin  urine.  But  this  latter  mifjht  easily  be 
attri!»uted,  as  Mrich  Meyer-"'  remarks,  to  a  kidney  injur>-  which 
interferes  with  its  secretion. 

A-ainst  the  idea  of  filtration  of  dissolved  crystalline  sub- 
stances bv  Glomeruli  and  secretion  of  coUoiil  compounds  by  the 
tubular  cells,  ajrain  are  Asher  and  his  pupils.^'  who  fovmd  no 
regularity  in  the  excretion  of  urine  uater  and  XaCl,  and  conclude, 
therefore.  s<>cretion  of  even  these  substances. 

Asher  furthermore  points  out  that  even  si,ecific  jrlands.  like 
the  salivary,  show  a  proportionate  relation  -f  dissolved  blood 


4(» 


HUKillT  S    DISKASK 


const  it  lUMits  Mild  water.  Hut  it  must  ho  nMiiniihorod  that  no 
other  i)ur(>  inland  res|)oiids  so  instantly  to  chaniLK's  in  the  con- 
centration of  tlie  lilood. 

Finally.  IJich  >h'yer.-'-'  who  has  studied  very  carefully  the 
elimination  of  urine  in  (lial)etes  insipidus  and  other  polyurias,  is 
of  oi)inion  that  this  urin(>  caiuiot  he  rejiarded  as  a  filtrate  of 
hlood-seruin.  inasmuch  as  it  is  too  dilute  as  reuards  its  total 
concentration,  hut  as  reirards  urea.  al)out  ten  times  as  concen- 
trated. For  instance,  in  a  case  with  a  total  urine  amount  of 
SdOlt  c.c.  and  a  nitrojieii  excretion  of  1 1  fim.  pro  die.  the  percent- 
ajic  of  ur(>a  contents  would  l)e  ahout  OM.  while,  according  to 
(iottliel).  the  hlood  only  has  a  concentration  of  ().((3  to  O.Oo. 
On  the  other  hand,  tlie  ("1  content  of  this  urine  was  on  some 
days  almost  ten  times  less  than  th;it  of  the  hlood.  He  further 
foiuid  that  the  diuretic  thef)cin.  j)roduced  in  diahetes  insipidus 
an  increase  of  concentration  without  increase  in  (piantity.  hut 
this  could  not  l)e  explained  l)v  a  disturl)anee  of  resorption. 

Similar  to  the  modernized  conception  of  Ludwijr  are  the  ideas 
of  Koranyi.-'  whose  view-  I  will  mention  in  detail,  hecause  they 
acipiired  considerahle  practical  importance. 

He  helieves  that  the  nUmieruli  filter  only  water  and  sodium 
chlorid.  hut  that  in  the  tuhules  occurs  an  eciuimolecular  exchangee 
with  metaltolic  products:  a  purely  phy.sical  process.  The  so- 
dium chlorid  of  the  urine  is,  therefore,  inversely  pro|K)rtional  to 
the  amount  of  nitrojien.  Based  upon  this  fact,  which  is  actually 
found  in  a  numher  of  conditions,  he  e.stal>lished  the  so-called 
urinary  (|Uotient.     This  is  ohtained  hy  dividin<>;  the  freezinjj- 

point      of  the  urine  hv  tlie  amount  of  sodium  chlorid,  .,  ,.,  = 

.\a(  1 

urinary  (juotient.     This  (juotient,  in  Koratiyi's  opinion,  depends 

upon  the  rapidity  of  flow  of  hlood  throujih  the  kidneys:    With 

diminishe<l  flow  the  (piotient  is  hijrh:   vice  versa,  with  inerea.s(>d 


STIU  (Tl  HK    AM)    KINCTIONS   OK   THK    XOKMAI.    KIDXKY       41 


flow  the  (Hiotient  is  low.     This  litis  1)(>(mi  found  correct  in  cases 
of  heart  disease  with  faihire  of  compensation  and  (rdenia. 

It  is  interestinj:  to  know  that  in  ciises  of  orthostatic  or  physio- 
lofiical  allnnninnria  the  (piotient  has  been  found  hijih.  very  much 
as  in  circulatory  disturliances.  while  in  true  nephritis  with  all)U- 
minuria  it  was  aliout  jiormal,  provided  no  chanjie  in  heart 
compensation  occurred.  It  has,  therefore.  Iieen  ur<ied  to  en)|)loy 
this  method  for  differentiation  of  orthostatic  and  nephritic 
all)uminuria.  Here,  ajiain.  repeated  invest ijrat ions  have  been 
vniahle  to  maintain  what  was  orijiinally  claimed.  Muller,  for 
instance,  states  that  it  fails,  particularly,  in  the  convalescence  ( :f 
pneumonia,  as  well  as  in  diabetes  insipidus,  when  the  percentafie 
of  chlorids  and  achlorids  rises  ami  falls  synchronously. 

One  fault  of  these  theories,  as  in  the  old  conceptions  of 
Ludwifi's,  is  their  disrejrard  of  the  metal)olic  activity  of  the 
kidney,  besides  elimination  of  preformed  nitro<tenous  waste- 
products  from  the  blood.  This  must  certainly  be  carried  on  l)y 
the  tubular  epithelium,  and  the  products  discharfjed  by  them 
into  the  tubules.  Moreover,  analysis  of  anatomical  and  physi- 
ological (>vidence  indicates  that  the  production  of  urine  can  not 
be  resartled  as  one  uniform  process.  This  complexity  un- 
doubtedly accounts  for  the  many  in  parts  conflicting  observa- 
tions and  ojMnions. 

In  the  production  of  urine  there  appear  to  be  concerned  two 
processes:  The  first  is  transudation,  and  the  second  secretion. 
The  structure  of  the  <:lomerulus,  as  well  as  what  we  know  of  its 
function,  supports  the  contention  that  we  have  here  a  proc-ssof 
transudation.  (Recently  Brodie  has  further  emphasized  the 
fact  that  the  glomerulus  acts  a  good  deal  like  a  piunp;  by  virtue 
of  the  elastic  capsular  fibers  the  filtered  water  may  be  put  under 
high  pressure,  in  which  it  is  aided,  of  course,  by  the  abrupt 
narrowing  of  the  tul)e  below.  Thus  it  flushes  away  the  secretion 
of  the  epithelial  cells. ^     That  the  glomerular  epithelium  is  secre- 


ll 


4J 


HUnilir's    DISKASK 


tory  sccius  iinpn)l»:il)lc.  for  the  reason  tliiit  it  only  partly  covers 
the  -loinenilws.  tliat  it  has  not  the  morphotic  character  of  secre- 
tory cells,  and  that,  under  pathological  conditions,  water  dis- 
charu-e  continues  after  its  loss,  unless  there  is  a  mechanical 
obstruction  to  its  outflow,  or  the  tuft  l)econies  diseased.  This  is 
|)articularly  well  illustrated  in  cases  of  contracted  kidney,  and 
in  some  cases  of  stasis,  when  the  epithelium  has  been  lost,  hut 
the  tuft  itself  remains  an<l  still  functionates.  It  isfiu'ther  corrob- 
orated by  the  fact  that  the  reaction  of  the  jrlomerular  product 
has  i)een  found  alkaline,  and  that  on  increased  diuresis  the  urine 
becomes  alkaline,  and  lastly  by  the  constant  i)resence  of  vary- 
ini:  faint  traces  of  serum  albumin  in  all  urines.  The  jrlomer- 
ulus.  therefore,  is  that  orfiaii  whose  duty  it  is  to  re>>ulate  the 
concentration  of  the  blood. 

Xow.  we  must  remember  that  this  water,  which  is  furnished 
by  the  proce.ss  of  transudation  from  the  <:lonierulus,  is  modified 
on  its  way.  That  modification  cannot.  I  believe,  be  explained, 
at  least  at  present,  on  a  jihysical  basis.  We  must  as.sume  that 
the  ei)ithelium  of  the  convoluted  tubules,  as  well  as  that  of  the 
other  tulniles,  plays  an  active  part  in  the  modification  of  that 
Huid  to  urine.  The  reasons  for  it  are  these:  The  osmotic  pres- 
sure of  the  uriie  is  nnich  hiiiher  than  that  of  the  blood,  and  it 
contains  specific  .substances,  and  in  such  varying:  amounts,  that 
an  active  part  of  these  epithelial  jrlandular  cells  is  made  most 
proi)able.  It  is  undoulttedly  for  this  reason  that  the  blood  is 
furnished  to  the  epithelial  cells  of  the  tubules  in  a  much  more 
concentrated  form.  The  chan<:e  from  alkaline  blood  plasma  to 
acid  urine,  however,  can  be  explained  on  physical  basis. 

The  anatomical  arran-rement  of  the  tubules  indicates  that 
there  must  be  stajination  of  the  transuded  water  in  the  con- 
voluted tul)ules.  This  may  be  for  the  sake  of  water  re.sorption, 
but  to  me  it  is  rather  more  for  the  purpose  of  complete  solution 
of  nitrofienous  elements  disciiarjied  by  the  epithelium   of   ihest- 


STKIC  TIHK 


AM)    KlNi  TIONS   OK   THK    NOltMAI.    KIDNKY        43 


tul)ul(>s.  This  is  ill  harmony  with  the  ()l)scrvati()ns  made  in  «'y- 
anosis  of  th(>  ki(hn\v,  wlioro  thourino  water  is  diminished,  but  the 
nitrogenous  <-ontents  ahout  normal.  On  account  of  the  venous 
stasis  less  water  transudes  through  the  jilomeruli,  hut  the  func- 
tions of  the  epithelial  cells  are  carried  on  profHTly.  until  they 
1,,-in  to  sutTer  from  nutritive  disturbances.  The  urine  is.  there- 
foiv.  concentrat(>d.  -V  theory  of  exclu.sive  water  resorption 
would  hardly  account  for  this  phenomenon. 

It  is  also  possible  that  water  resorption  occurs  only  when  the 
am(.vmt  of  transuded  water  exceeds  certain  limits.  We  must 
,.„nfess  i-norance  of  the  specialized  functions  of  the  various 
parts,  and  types  of  epithelial  cells.  comiK)sinji  the  tubules,  ami 
of  the  details  of  the  secretory  act. 

A  f(.w  words  about  the  discharge  of  the  urine  from  the  pelvis 
of  the  kidnev  into  the  ureter  and  bladder.     The  physiolo-ical 
text-books  leave  us  in  the  dark  about  the  mechanism  of  this 
process,  althoujih  we  are  informed  that  the  urine  is  propelled 
by  active  contraction  of  the  ureters  into  the  bladder,  and  that  a 
return  flow  from  the  i)elvis  into  the  tubules  is  made  impossible 
bv  compression  of  the  tubular  orifices  by  any  increase  in  pelvic 
pressur(>.      Both  pelvis  of  kidney  and  ureter  have  essentially 
the  same  structure;    they  are  stronji,  elastic,  muscular  orjians, 
lined  bv  nuicous  membrane,  and  it  api)ears  probable  that  the 
activ(>  waves  proi)ellinj:  the  urine  throujih  the  ureter  into  the 
bladder  take  their  orijrin  in  the  pelvis  and  similarly  force  the 
urine  into  the  ureter.     This  has  for  us  considerable  interest. 
In   manv   lonji-cotitinued   diseases,   but    notably   in  the  senile 
kidnev.  there  occurs  marked  weakening  of  the  elastic  muscular 
layer  of  the  iM>lvis,  with  the  result  that  this  gradually  dilates  to  a 
c(indition  of  hvdronephrosis.  although  no  mechanical  obstruction 
outside  of  the  kidney  exists,  and  the  ureters  ami  bladder  are  not 
dilated.     In  these  cases  the  jK'lvis  evidently  loses  its  power  of 
active  tli.schar>ie  into  the  ureter. 


;} 


44 


UHltiin's    DISKASK 


I  hclicvc  lliiit  this  covers  as  much  as  \\v  arc  justified  to  assume 
at  i)resent  almul  the  secretion  of  urine.     Much  is  still  uncertain 
and  contradictory.     We  confess  its  d(>ticiency  and  uncertainty, 
and  there  exists  ;:reat  ditficulty  in  the  ap|)ncation  of  the  experi- 
mental physiolojiical  knowledge  for  the  explanation  of  diseased 
fimcti<»ns.     In  this  connection.  I  would  like,  however,  to  empha- 
size '-ertain  points,  which  may.  at  least  to  some  dejiree,  account 
for  these  discre|)ancies.     It  appears  that  we  are  vmahlo  to  tran.s- 
pos(>  directly   physiolo<ii<':d   knowledjre   for  the  explanation   of 
pathol(    ical  phenomena  for  the  followin«!:  reasons:   The  patho- 
lojiical  oriran  is  essentially  a  different  or<:an  from  the  normal.     It 
presents  n\ore  than  simple  alterations  of  physiolojjical  proees.s(>s. 
in  exajijieration.  diminvition.  or  aliolition  of  certain  fvmctions 
which   depend   on   similar  or<ranic    chanjies.     It    is    really    iti- 
comparaltle   to   the    normal   orjian    from    which    it    developed. 
Its  whole  architectural  arranjrement  is  chaiified  l)y  the  formation 
of  new  tissue  and  the  introduction  of   new  cellular   elements; 
its  channels  of  nutrition,  lymph,  and  nerve  distrilmtion  l)ecome 
fundamentally  altered;   secretory  ducts  are  lo.st ;    new  ones  are 
created;     new   cell   types  develop  from    the    prei'xistinj:   par- 
enchyma cells;    in  short,  the  patholofiictd  orjian  is  a  new  one, 
characterized  l)y  tissue  of  its  own  and  sjH'cific  arranjiement  of 
its  parts.      \o  wonder,  therefore,   that    it    presents   functional 
phenomena,  which  cannot  he  fully  covered  or  explained  by  a 
direct  application  of  the  results  of  simple  physiological  ex|)ori- 
mentation  and  consideration  derived  from  the  normal  orj;an. 

Here  is  a  future  field  for  patholojjical  anatomy.  It  can  no 
lonjrer  he  satisfied  to  descril»e  and  disclose  h'sxKc  charKjcs,  hut  it 
nuist  construe  the  plan  of  the  whole  pnthohmivdl  oiyati.  Only 
a  kiiowledfie  of  both  will  ultimately  lead  to  an  intelli<:ent  under- 
standiiifi  of  patholojrical  fimctions  of  a  whole  orjian.  and  estab- 
lish a  patholojrieal  physiolojry  commensurate  with  the  normal. 


THIHl)  LKCirHK* 

Thk  Dkcknkuativk  and  KxiDATivK  Fkatikks  ok 
Nki'HIutis 

<ii  nth  fii(  n: 

I'ollowiufi  the  classification  iiulicatrd  at  the  end  <»f  the  first 
ItM-tuiv.  I  Uiru  to  a  dotailcd  description  of  nephritis  simplex.     I 
understatid  by  it  a  diffuse  inflammation  of  the  kidney,  charac- 
terized   l)y    parenchymatous    de-ieneration    and    n»flammator>' 
(edema;    that    is,   serous  exudate   with   diminished   resoq^tive 
:,l,ility.     This  type  of  kidney  lesion  is  now  variously  classified  as 
:.cute  nephritis,  or  acute  parenchymatous  nephritis,  or  acute 
parenchvmatous  defeneration  of  the  kidney.     The  impropriety 
„f  the  first  two  terms  I  have  already  covered,  hut  i  am  ohlijred 
t„  pav  some  attention  here  to  the  last,     the  acute  parenchyma- 
tous ile-enerationof  the  kidney,     inasmuch  as  stronjr  attempts 
irive  l)een   made,  onlv   <iuite  recently  ajrain.   to  separate  the 
degenerative   lesions  of   the   kidney    fron.    the   inflammations, 
rids  has  been  stronjjly  advocated  by   MuUor.'  who  wants  to 
substitute  the  term  nephroses  for  all  such  non-inflammator>-  but 
essential  de-enerat ions. and  Marchand.and  L()hlein  and  Heineke." 
with  some  others,  look  more  or  less  favoral)ly  upoji  such  classifi- 
cation.    The  evidence  for  it  is  that  there  exist  some  diseases, 
cholera  foremost,  and  some  intoxications,  like  those  of  phos- 
phorus, chromium,  and  corrosive  sublimate,  in  which  extensive 
parenchymatous  dejreneration  occurs  primarily  and  i)rominently. 
which  mav  or  may  not  become  associated  later  with  inflamma- 
tory henu)rrha-es  and  cellular  exudate,  and  finally  with  pro- 
ductive interstitial  chanjjes. 

•  Dclivrml  on  l'cl)ru!iry  4,  HKK). 
45 


HHMiins    KISKASI 


M;iirli:iiiil.'  s|M';ikiiin  <»f  the  kuliH-y  chriiim's  ill  (•(•rnwivo 
siihliiM.itc  iMtis<ttiiii^',  nrjiucs  tli.il  nuv  is  not  justiticd  in  n'^nnliiif: 
the  iiiili;il  lesion  as  a  iicpliritis.  iiiasinucli  as  the  dcm-iHTation  is 
the  (lirctt  priman  cHVct  of  the  ixtisoii.  aii<l  that  death  or  «•- 
generation  may  occur  witliont  additional  infianinuitory  reac- 
'I'liese  latter,  he  holds,  are  only  the  late  n'sult  of  a 
1  liv  the  auMiniul.ilion  of  ne«Totic  cell 


1lon^ 


cheniotaclic  action  caiis<M 


niaH'tial  and  not   reduced  by  the  iMiistm  its<'lf.  which  has  lonjj 
before  ceased  to  exert  its  influence. 

Hut  Marchand  himself  admits  ;;nd  this  is  very  evidertt  to 
any  one  reading:  the  ,escriptions  of  lleineke's  cases  of  corrosive 
suMiinate  kidneys  that  the  hsion  is  as.sociated  from  the  .start 
with  consideralile  sentus  d-dema:   he  attributes  this.  howev(>r,  to 


a  iion-indammatorv.  increased  capillary  jM-rinea 


ibilit^ 


an( 


li 


)()S- 


sible  h'ssened  resorption,  a 


nalojrous  to  the  amvloid  kidnev.  and 


)ases    this   view    on 


the    absence   of    hy|M'ra'mia   and    hemor- 


rhaues. 


It  is  ditliciilt  to  follow  this  attempt  of  a  finer  chi.ssificati<m  in 
either  substance  or  form.  In  readin<r  over  the  careful  work 
of  Heineke  on  the  subject,  it  aj)pears  that  the  lesion  presents  it- 
self primarily  as  a  marked  parenchymatous  dejieneration  with  in- 
flammatory (I'dema.  followed  soon  by  a  cellular  exudate  and  later 
by  imxluctive  interstitial  chaiijies.  To  sharply  separate  the 
primary  parenchymatous  dejreneration  from  the  accompanyinj: 
(edema,  and  a^'ain  the  almost  immediately  followinj:  cellular 
exudate,  seems  to  me  somewhat  forced,  and  ba.seii  on  theoretical 
considerations,  which  are  op<'n  to  some  critici.sm.  Who.  for 
instance,  in  the  inflammations  of  the  hmj:,  would  rejraril  the 
initial  (edema  which  prec(>des  the  cellular  exudate  as  non- 
inflanunatory.  and  ^genetically  unrelated  to  it? 

The  absence  of  general  hypera'mia  and  hemorrhafies  cannot 
be  taken  as  proof  ajrainst   the  inflammatory  character  of  the 


I)K<iKNKKATIVK    AND    KXIDATIVK    KKATl  HKS   OK    NKI'HHITIS  47 

lesion,  inasmuch  as  any  inflamed  or^an  with  much  swelliri):  and 
iiiflatnmatorv  n'denia  of  its  parts,  is  jienerally  antenue.  Furth«'r- 
int>re,  it  apjM'ars  from  Heineke's  description  that  in  early  cases 
•  the  cortical  capillaries,  the  ;:lomerular  tufts,  and  the  medullary- 
capillaries  showed  frecpieiit  ai)undant  l»l(»od  injecti<m."  iS<'e 
particularly  his  Case  I  of  seven  hours:  "The  glomeruli  dark  red, 
(■•lually  the  peripheral  |)orti(ms  of  the  pyramids." ^  I  can 
inter|)ret  this  only  as  an  inflammatory  hyiM-ra-mia.  This,  of 
course,  JM-comes  lessened  ami  more  irregular  as  swellinn  and 
inflammatory  (i'<len»!i  projiress.  Further,  it  is  no  a  priori 
certainty  that  the  appearance  of  the  cellular  exudate  dejjends 
only  u|M)n  chemotactic  action  of  necrotic  cellular  mas.ses. 
Other  factors  may  enter  into  this,  the  discu.ssion  of  which,  how- 
ever, would  lead  us  too  far  from  our  topic. 

I  feel  unconvinced,  therefore,  that  we  are  justified  in  estab- 
lishiufr  an  indejx'ndent  catej!:or>-  of  nephroses  or  parenchy- 
matous dejrenerat  ions  inde|X'ndent  of  inflammations,  as  .MuUer 
would  have  it.  Indeed,  even  Marchand  is  quite  con- 
scious of  the  additional  difficulty  thus  introduced,  for  it 
would  still  become  necessar>-  to  afiain  apply  (lualifyinfj  adjec- 
tives. How  nmch,  for  instance,  wo»ild  l)e  <iained  by  sjx'akinji 
of  parenchymatous  or  dejrenerative  nephrosis  or  of  an  inflamma- 
tor>-  nephrosis?  The  latter,  particularly,  would  soon  lead  back 
to  a  confusion  from  which  we  are  oidy  t(K)  anxious  to  e.scaix'. 

We  will  therefore  not  recognize  in  our  study  a  non-inflam- 
matory, parenchymatous  defeneration. 

\ow.  to  return  to  the  discu.ssion  of  simple  nephritis:  It  is 
the  form  which  is  mo.st  frequently  found  in  connection  with  all 
t.\  pes  of  fevers,  such  as  typhoid  fever,  the  early  stages  of  scarlet 
fever,  synanche  infections,  cholera,  septica'mia.  and  others.  It 
also  (»ccurs  in  toxic  and  cachectic  states  and  in  .some  ixiisonings. 
Such  a  kidney,  firo-ssly.  varies  little,  if  any.  from  the  normal 


4S 


iii(i(inr°>^  hisKASK 


n'v/.v.  Itiit  :i|)|H'!ir!<  swollen 


riic  fiipsiilr  i>  stivtihnl    lluii,  l»tH 
„'lH^  strilMM-il  otT  will.  .-MS.-       riu-  suifa.T  l.uk,.>,  m.uI  this  ran 
fivtiiinitlv  Ik-  srni  im<lcr  llu-  lliin  «-.<|"*"' 


it  In  siitnotli.  :iiiu  un> 


UsumUv  :i  SOI 


1  of  iliiskv-^'niy.  pinkish  color. 


lliMl.  howcv.'r.  is  o|MMi  I..  ">in.-  v.ni.-itions; 


<  )cc.isioii;ill\ .  IIk' 


surf: 


ic«'  in; 


,v  show   .lislincl   Miras  (.f   vas.ul.n    iiijc-tion,  l.iit   <.u 


iccol 


lilt   of   the   iHTSsiin'  ( 
fwial 


•nfhvina,  lln'  siipci 


,1    tlir  swollen   aixl   (j-^lcin.ilous   par- 
veins  aiv  iisiiallv  not  at  all    .roinineiit , 


and  soinctiincs  ca 


nnot  lie  tnatlc  out   iit  al 


ap|M>ai 
of  uiu'(|U: 
coinpcnsatoiy   • 


.\::ain.  th«'V   in:iy 


•ount 


moir  prominent  in  itla.rs  an.l  l..st  in  ..th.'-.  .-n  a(( 
I  (list ril.ut ion  of  inllaininatury  ••hjinyes  and  r(,ns4-(|uciit 


•liaii>;< 


in   the  Mood-sticimi.     <  'ti    m'cIioii. 


th 


kidiH'v  shows  roiiditions  siin 


ilar  to  tlios<'  oliserx-ii  on  uross  ex- 


am 


illation.      The  cortex  :i 


I 


liromineiit. 
ir  rows,  ins 


he  markinu? 


Iwavs  liuliies  and   ap|)eaiv  rehitively 
show  irreuulnnties  and  tlie  -lomeiii- 


tead  of  presenting;  a  v( 


•rv  dehnite  arraiiiieineiit .are 


distorted.     The   -lomeruli  apiK'ar  in  s,M.ts  very  prominent  on 
,t  of  a  very  marked  vascular  injection,  and  in  others  they 

n  he  recojiiiized  in 


accoui 


inav 


have  disa|)i)eared  alto-n'ther.  or  they  ca 


en 


;h.  slisihtly  elevated  points.  They  se<>m 
Ik.  rais(.d  ov.-r  the"  surface  of  the  cortex.  Such  rows  of  jilom- 
,li   are  .separated   l.v    tlii.-k.   j;ray.   swollen,   tulmlar  masses. 


the  form  of  fine,  irrayi 


to 


Occasionallv.  one  can  .s.,ueeze  from  the  ki<lney  a  certain  amount 
of  .e.lematous  flui.l:    this,  h.mever.  deiHMids  entirely  upon  the 


late.     Where  all  of  this  has  been  imbibed 
l,v  the  structures  of  the  kidney,  it  may  even  1h'  dry  an.l  firm 


amou 


lit  of  s(>rous  exu( 


Similar  conditions  preva 


(I 


il   in   the  medulla.     The  me«lulla, 

ijr  dear  and  dehnitely  striated,  is  rather  dull, 

The  medullary  rays  are  prominent,  pale,  and 

di'inatous,  while  the  interp<)lat<>d  vessels  are  for  this  rea.son 


instead  of  appearin 
uravish,  swo 


.lie 


obscured  or,  for  compensatory  re 


esse 
isons.  apjM'ar  in  places 


much 


more  prominent    than   they  on 


linarilv   do   iVvA-    l>-     Pressing: 


I  is:  1  .\i|iliriii>  -iinplrx,  frnin  pntTjiI  sent  ioirmia  fi)llii«in);  niiildlc-c.ar  .lis.  asc. 
(  l..u.lv"-u.lliiiL'  aiiil  MToiis  iMi.lal.'.  Si.iiic  iif  tlic  (rlimiiTuhir  rows  with  iiillamnial.iry 
.ni'nri.'iiiuiit,  tint  grmmllv  llic  cortieul  ii\:irkiii(rs  l.>sl  i.r  .lislurlx.l  Uy  cli.mly  sw.  Iliu);  uiul 
-mills  cMi.lali.m  into  ilir  parts.  Similar  -late  in  tlic  m.'.liilla.  Mu  ri>»r.ii.i<  allv,  tins 
ki.lii.  y  showi.l  IK)  (illiilar  or  liliriiiiius  !>sii.latiiiii,  li\it  iIdii.Iv  ^«illiiitf  "I  nils.  v«,  Ihiiir  of 
irl.."!.  lular  I'li.lotli.liiiin  an.l  cintlicliuin,  ami  .s<n)Us  cvinian  iiim  tin-  ;;ioiini  uiai  >ii|»ulo 
aii.l  iiilirstitial  tlHsiii'.      Wciulil,  2.')0  Kius. 


■In! 


I)K(iKXKUATIVK    AND    KXIDATIVK    FKATIKKS    OK    NKI'HKITIS      49 


ifli 


I 


Mi. 


I'in.  2.  Ncplirilis  siinplcx:  Iiifltinmiiitorv  <'i)|i()r({cnn'nt  iif  glonH-nilar  capiUarifs,  with 
nciicr.il  .•iilaiKrmtMl  of  the  tuft,  ilouilv  swi'lliuK  of  its  i-iidotliclimii  and  cpil helium;  the 
liilUr  parllv  <lrs(|iiaiiialnl.  ( Iniiiuhir  clisiutcKnition  of  the  capsillsii  rpitlioUuin.  Occa- 
>ioiial  nuto'rtji'miMit  of  iiili'ituliular  <ii|)illarics.  Clouily  swcUiiiR  ami  granular  ilixiiitcuni- 
lioii  of  tiiliiilar  rclls,  with  occasional  miclcar  (IcKciicratioii. 


M 


I)K(;i-;m;i{ativk  and  kxi  dativk  kkatihks  of  nkphhitis  ol 

•rctitly  on  tlio  iiioduUa  toward  tho  |M'lvis.  we  aiv  frociucntly  ahlo 
to  (liscliarfic  from  the  papilhr  a  sli<:htly  turhid  fluid,  ami  on 
cxaininatioii  that  fluid  is  found  to  consist,  to>rn'at  extent,  of  des- 
(juaniated  tubular  epithelium.  This  leads  us  to  the  mieroscopic 
aj)|K>a  ranees. 

We  observe,  here,  certain  variations  from  the  normal,  which 
are  more  or  le.ss  evenly  distributed  throujih'>ut  the  whole  kidney 
substance.  In  the  sinii)lest  :ind  earliest  f(..'  .s,  the  more  promi- 
nent features  are  turbidity  of  the  jjlomerular  tuft,  .serous  exuda- 
tion into  the  jrlomeruli,  and  a  parenchymatous  de<ieneration  of 
the  epithelium  of  the  convoluted  tubules.  The  jrlomerular  capsule 
ap|H'ars  usually  i|uite  larjje,  and,  in  the  well-establi.shed  cases, 
surr(»unded  by  o'dematous  tis.sue.  The  epitheliimi  of  Bowman's 
capsule  is  turbid,  and  so  is  the  epithelium  which  is  reflected  over 
the  }ilomerulus.  In  a  certain  munber  of  "ilomeruli  the  capillar}- 
tuft  is  very  markedly  injected;  in  othei-s,  inflammatory  swellinji 
and  turbidity  of  the  capillary  endothelium  evident  and  soon 
followed  by  a  serous  exudate,  so  that  the  <:lomerular  tufts  apix^ar 
thick  and  plump  and  fill  the  capsule.  In  this  way  jilomeruli 
firadually  lose  their  hyjH'ra'mic  form.  Then  a  .serous  exudate, 
demonstrable  by  its  coajrulatinji  on  hardeninfr,  can  1)0  seen  in 
Bowman's  cap.sule.  If  that  exudate  assumes  any  marked  dejiree, 
the  tuft  is  con»press{>d  by  it,  and  thus  its  circulation  necessarily 
nuich  interfered  with.  If  this  process  a.ssumes  any  dimensions, 
tlie  capsule  Inn-omes  dilated,  while  the  tuft  itself  is  further  pres.sed 
ajrainst  one  part  of  the  capsule,  usually  at  the  entrance  of  the 
vessels;  such  jilomeruli  ap|M>ar  then  as  the  fine,  slifihtly  elevated, 
pale,  <!:ramjlar  dots,  noticeable  on  the  cut  .surface  of  the  cortex 
'  I'ijis.  2  and  ."ii. 

In  the  majority  of  cases  of  simple  nephritis  that  point 
is  not  reached,  at  least  not  in  the  majority  of  jilomeruli,  and  they 


uiiHiin's  DisKAsi: 


rciiiiiiii  lurl>iil.  swollen 


IIK 


1  the  cMpillMiy  Wiills  thick,  piilc.  :itnl 


pluiiip 


Tlic  I'h.iii-cs  111  tl 


lie  (  i)itlicli:il  fdis  of  the  convoluted  tiiitiile 


re  more  evitlcn 


t   at   lirst   si-iht   tliiin  the  ch;in,i:es  tountl  m  tl 


Malliiuhiaii  coipusi 


Thev  consist  of  varvinii'  deiifees  ot  pai 


eiich\  nialous  i 


niatoiw  (leLl<iirlatloii  is  Ml  1 


lal  study  ol 
with    the  e 


Mut   it   iiia>    no 
you  tile  present 


l,.oviieratioii     Fi-.    \k     The  nature  of  pnivnchy- 

tself  a  very  important  and  fundainen- 

lolo-v.      I  take  it  that  you  are  familiar 


iciieral 


patl 


sint'ial    '■•alures  of   it    from  your  previous  sttidies. 
t  l)e  amiss  if  I  shortly  summarize  once  more  for 


knowled-:*'  reiiardin.!:  it. 


itl 


otiieif 


■rh(>  kidney  from  the  time  o 
the  favored  ori:aii  for  inve 


f  \ircho\v  '  has  lieeii,  above 


paieiu 
nature 


express  U( 
structures 


^ranuk 


■itijiations  into  the  character  of 

■hymalou.-.   d.-uciieration.     Virchow.    whose   ideas  (m   its 

1   h.ive  already   presented,   introdiK-ed   the  appi'opiiate 

f    'cloudy  .swellinii":    and  these  two  words 

^uch  cells  lose  their  definite  normal 

iiul  outline.     The  delicate,  rod-like  striation.   com- 

lar   arranuement    of   line   .■iiamiles   i.Xltmann's 

u  rnnemher.  forms  a  feature  of  the  jho- 


descriptive  term  o 


llit^ 


nneaiaiice 


(sed   of   a    fciiu 


WlllCll. 


as  vo 


,lasiii   of   the  cells  of   the   convoluted   tuhules.   becomes  <lis- 


toi 

turbed.  irreuular.  the  -iranules  more  numerous,  coarser,  a 


IM'omineiit  :  the  c»>ll   as    a    whole    appears   ( 
brushe(l  extremity   may 
succulent,  swolh 


larker. 


nd  more 
finelv 


(hist 


be   lost.     The   cell    enlariics.    appeals 

n.   turliid.   and   plump-  :""•  occasionally   as   if 

(Ml  with  -raiiules.     This  has  ,i:iv(Mi  rise  to  the  term  -  irranular 


de>reneration.'"     These  lifanules  are  iiiso 


luble  in  chlorofoiin.  ether, 


1  alcohol,  but    soluble   in   acetic  acK 


1  and  weak  alkalis,  and 


have  therefore  been  re<iarded  as  of  an  albuminous  character. 
'Ihere  may  be  t)resent.  however,  other  lar;.i(>r.  hyaline.  ;rlol>ular 
bodies.      Thev  aiv  rejrarded  by  some  as  the  product  of  a  i)ath 


olojiica 


1  secretion.     I  shall  say  more  a 


bout  these  in  the  discu.s- 


)K(iK.\KI{.\TIVK    AM)    KXri)ATI\  K    KKATIUKS    OK    NKIMIUITIS   ii'.i 


KitJ.  :t. — Ncpliritis  -implrx:    ( ilmnciuhir  capsiili'  ilistciidiMl  liy  sitiiiis  cxui 


lair.     Th. 


lufl  iDiiipirsscil  .mil  ailliiicnl  to  i):irt  of  the  capsular  wall,  wIium-  cpilliclii 


■  III  IS  ri'lalivrly 


well  prcMivcil;   ildiidy  swclliiiK  ; 


I  (i-iliiiia  (if  siirroiiiiiliiin  struct  arcs.      X  "JIO. 


l.'i^.  4. — (iranular  illsiiilc(£ratiim  iif  coiivolutcil  lulmli's.     A  better  prcscrviil  loiiii  of  Hcnlc. 


II 


|)K(iK\KU.\TIVK    AM)    KXl  DATIVK    KKATIHKS   OK    NKI'HHITIS   ")') 

sioM  of  tube-casts.     Tlic  imclous  is  |)rimarily  imaffoctotl.  ami  is 
involved  only  in  progressive  and  severe  lesions.     Its  chaiifies  are 
those  of  chroniatolysis.  /.  r.,  a  centrifufial  lo.ss  of  ehromatic  sub- 
stance, and.  as  Benario"    holds,  are  similar  to  those  ol)serve<l 
within  the  jmjtopla.sni.     The  outcome  of  this  form  of  defjenera- 
tion  varies.     In   the  simple  nephritis,  when  the  nucleus  is  not 
destroyed,  restitution  to  intejirity  is  probably  the  rule,  /.  r., 
the  majority  of  cells  recover.     Others,  however,  may  }io  on  to 
complete  destruction,  the  cell  membrane  IxM'omes  lost,  and  the 
protoplasm  disintef>;rates  into  a  «rramilar  detritus  and  dissolves. 
When  such  severe  chanfies  are  absent,  but  the  parenchymatous 
destruction  continues,  the  apjM'arance  of  fatty  siib-stances  l)e- 
comes  pronovmced.     1  shall  leave  the  discus.sion  of  this  subject  to 
a  later  date,  when  we  are  dealinjj  with  the  fatty  type  of  nephritis. 
Opinions  about  the  nature  of  parenchymatous  defjeneration 
differ  widely.     It  involves  two  main  que.stions:    What  is  the 
derivation  and  sifinificanee  of  the  jiranules,  and  what  the  orijrin 
and  sifinificance  of  the  swelling  of  the  afTected  cells? 

Both  were  easily  explained  by  Virchow's  conception  of  over- 
nutrition  of  the  cells.  Only  shortly  l)efore  his  death  Virchovv 
declared :  The  swellin^t,  as  well  as  the  cloudiness,  depend  uiK)n  a 
IM'rmanent  assimilation  of  soluble  substances,  which  are  pre- 
cipitated within  the  cell  and  underjjo  further  ehanjjes.  The 
swelling'  is,  therefore,  not  caused  by  the  usual  nutritive,  but 
by  changed  material." 

An  entire  chanjje  in  the.se  ideas  went  necessarily  with  those 
of  the  character  of  inflammation,  for  inasmuch  as  the  parenehy- 
nuitous  degeneration  was  no  lonfjer  considered  a  nutritive  dis- 
turbance, but  the  direct  result  of  an  injury,  it  l)ecame  necessarv' 
to  explain  the  cloudy  swellinji  in  some  other  way. 

It  has,  therefore.  l)een  variously  considered  either  as  a 
granular   precipitation   of   normally   dissolved   proteid    (Rind- 


it! 


r>(> 


UHKiMTS    DISKASK 


Hcisch.'  ("t.liiilicim"'.  <>r  as  a  coaiirulation  i  Klohs  "*),  or.  inoro 
■rciuMally,  as  a  (lisornaiiizatioii  of  protoplasm  with  resorption  of 
fluid  iZiculcr  "  i.  or  as  a  rcfrrcssivc  iiictainorpliosis  due  to  uiulcr- 
iiutritioii  Tlioma'-i.  Soiiio,  like  Bircli-Hirschfcld "  and  von 
Hcckliniiliauscn."  retain  partly  the  views  of  Virehow.  The 
former  Itelieves  that  it  represents  an  accumulation  of  undis- 
solved or  precipitated  i)roteids  as  the  result  of  increased  proteid 
destrviction  with  an  increased  supply  of  proteid;  the  latter 
rejiards  it  as  an  increased  functional  activity  similar  to  the 
increased  productioji  of  mucus  in  the  catarrhal  inflamnuitions  of 
mucous  meml)ranes. 

('onsideral)le  experimental  work  on  the  subject  has  l)oen  done. 
Schilliiifi ' '  obtained  cloudy  swellin^i  of  one  kidney  forty-eifjht 
hours  after  tyinj:  the  renal  vein  of  the  other.  He  concludes, 
therefore,  that  this  nnist  he  the  result  of  com|)ensator>'  action  on 
part  of  that  kidney,  caused  by  the  increased  amount  of  urinary 
constituents  in  the  blood,  a  forerunner  of  hyjK'rtrophy.  Land- 
stcMner,'"  however,  has  pointed  out  that  these  result.s  are  not 
identical  with  those  of  infections  or  intoxications.  The  cells  of 
the  first  convoluted  tubules  were  left  entirely  free,  and  the  lesion 
remained  strictly  localized  to  the  cells  of  the  proximal  convo- 
luted tubules.  This  is  the  very  oppo.site  from  what  is  usually 
ol)served  in  disea.se. 

Such  experiments  are  entirely  unconvincinji  for  exi)lana- 
tions  of  either  hyi)ertrophy  or  parenchymatous  de<>;eneration, 
for  the  reason  that  such  an  interference  suddenly  produces 
marked  complications  in  the  lanctions  of  the  other  kidney,  and 
to  such  an  extent  that  one  is  not  justified  in  drawing:  any  con- 
clusions from  it.  One  mijiht  interpret  these  results  as  moderate 
injury  to  a  particular  jrroup  of  cells  of  the  kidney,  caused  by  the 
.sudden  ( aanjies  in  circulator}-  conditions  and  th(>  increased 
amount  of  urine  constituents.     There  is  no  evidence,  as  far  as  I 


l>K(iK\KKATIVK   AM)    KXIDATIVK    KKATIKKS   OK    XKI'HHITIS  .)< 


know,  which  could  corrolwrnitr  the  view  that  parciichynmtous 
(IcjroiM'ratioii  hears  a  fienetic  relation  to  hyiMTtrophy. 

There  is  i»o  uiiiforinity  of  opinion  about  the  derivation  of  the 
jrrainiles.  While  some  l(M)k  upon  them  as  an  increase  of  the 
normal  tyiM'.  (ialeotti'"  holds  that  they  represent  a  ditTerent 
a^'v:i'<'>i:>te  condition  of  the  cytoplasm,  while  the  normal  <iraiuiles 
disapjH'ar.  Based  on  Xae<:eli's  theory  of  protoplasm,  he  holds 
that  the  protei<l  molecules  los<»  their  ability  for  the  formation  of 
micelhe,  which  are  the  fundamental  reipiisite  of  life,  and  the 
new  "iranules  thus  resultinji  represent  the  first  evidences  of  cell 
necrosis. 

It  will  l)e  seen  that  views  alniut  parenchymatous  degenera- 
tion are  larjrely  dejiendent  ujx)n  the  theoretical  conceptions  of 
protoplasm.  This  is,  i)erhaps.  best  illustrated  in  the  most  recent 
ideas  of  Alhrecht,'*  who  rejiards  protoplasm  as  an  emulsion, 
which,  under  various  influences,  particularly  water,  loses  its 
homofieneity,  and  chanjtes  to  a  mechanical  mixture  which  con- 
tains drops  of  one  substance  susjx>nded  in  the  other  (tropfifje 
llntmischunji). 

Based  on  his  own  studies,  Landsteiner '**  concludes  that  the 
process  is  essentially  a  destruction  of  the  filamentous  structure 
of  the  protoplasm  with  dumpinf:  into  jrranules.  The  swellinji  is 
to  l)e  attributed  to  the  destruction  of  the  protoplasm.  He  is 
inclined  to  attril)ute  the  whole  to  autolytic  processes.  Similar 
are  the  views  of  Orjrler  and  others,  who,  having!;  foiuid  substances 
of  the  myelin  jrroup  in  such  cells,  look  upon  it  mer(>ly  as  a  myelinic 
(le<ieneration.  or,  better,  disorganization  of  the  protopla.sm 
an  autolysis.  I  shall  say  more  alnnit  this  later  in  connection 
with  the  fatty  typ?s  of  nephritis. 

.\dami -' holds  to  the  possii)ility  of  increased  absorption  of 
food-stutTs,  with  imperfect  conversion  and  utilization  of  the  same, 
and  differentiates  it  distinctlv  from  granular  degeneration  or  the 


ii 


.')S 


HltKiin's    niSKASK 


•troplijrc  liiitiiiisclmn-.'"  nf  Alhn'clit .  'I'liis  lie  iv-tiinls  ;is  u 
.lisiiitci:i:itiv«'  (oii.lilioii  t»f  the  cytopliism,  an  iiidifatum  of  cell 
(Ifiitli.  mimI  alliftl  t<t  the  <:ranular  dcjinu'ralioii  drscrilH-d  l»y 
Vcrworii  in  injured  infusorians. 

In.in  my  own  ()l.scrvali<»ns  I  iK-licvc  that  tho  \mwvHH  de- 
pends u|Min  outside  infhiences  whicli.  either  !»y  exeessive  stinni- 
lation  of  the  cell  aetivity,  or  by  direet  harmful  influenees.  pro- 
duce (listurl)ances  in  the  e«»mi)osition  of  the  protoplasm  wliieh 
neeessarily  lead  to  chanjies  in  the  orjranization  of  the  parts,  and 
temiM.rary  or  |KMinanent  eell  injury.  The  ap|H'aranee  of  the 
-rranules  I  also  rejrard  as  an  indication  of  changed  protoplasmic 
constitution,  wherehy  the  normal  com|H»siti(m  and  arraiijrement 
are  uradually  lost:  and  I  attribute  the  swellinjr  to  the  thus 
.•titered  physical  conditions  of  the  cell  and /7.s<7uj/if/c«/«7(r(r«/(/m7(/. 
I  )ependin;:  on  the  dejiree  of  injury  and  the  correlated  disturbances 
in  the  protoplasm,  the  cell  either  adapts  itself  to  the  new  environ- 
ment or  ehan^M's  its  character  entirely  by  undernoinj:  further 
dejrenerative  (fatty  i  chaiifres  or  complete  disor;:anizution. 

I  have  endeav(>ro<l  to  recall  to  your  mind  these  fundamental 
l)rinciples  of  ^leneral  patholojiy  lH>cause  they  play  so  imiK)rtant 
a  role  in  the  correct  and  I'lear  conceptions  of  nephritis,  and  we 
will  have  to  refer  to  them  fre»iuently  in  our  subsefjuent  study. 

To  return  to  the  subject  of  simple  nephritis.  I  shall  only  have 
to  add  that  the  tissue  U'tween  the  tubules  shows  the  same  in- 
flanunatory  cedema  which  I  have  already  mentioned  in  connec- 
tion with  the  |H'ri«ilomerular  tissue.  It  is  stretched,  hazy, 
se|)arated  by  (edematous  fluid.  The  intertubular  capillaries  are 
in  parts  enjiorjred  or  may  1h>  compres.sed. 

The  result  of  simple  nephritis  is  restitution  to  integrity  in  the 
majority  of  ca.s<'s.  The  inflammator>-  (rdema  subsides  and,  after 
clearinji  of  the  lymphatics,  is  re.sorl)ed;  the  filomeruli  and  the 
vascular  apparatus,  not  havinji  underjione  jjermanont   injury. 


DMiKNKUATIVK    W       KXIDATIVK    KKATI  HKS   OK    NKniHITIS  .W 

MssuiiM'  their  fornu'i  comlitiMn.  Tho  cpitlioliuin  also  rcjU'iiiTati's 
ra|)i(lly.  iiiasinucli  as  (.nly  littl«-  of  it  has  undcruono  actual  necro- 
sis, and  the  ki<hicy  n>ay.  therpioro.  !)<■  said  to  recover  coinph'tely, 
iniless  conditions  su|)ervene  which,  prolon^'ing  the  interference, 
liradually  lead  to  tlie  more  severe  tyj)os  of  kidney  infianunations 
wiiich  I  am  now  ahout  to  descril)e. 

licfore  that,  howt  ver.  a  few  words  alM)ut  the  functional 
clianjjes  in  these  casi's  of  simple  nephritis.  The  structural 
clian}.>es  in  the  vas«ular  apparatus,  as  well  as  the  mechanical 
conditions  in  the  swelling  of  the  parts,  result  necessarily  in  a 
much  din.iiiished  aniount  of  urine,  of  relatively  hijih  ccmcentra- 
lion  and  .--H^cific  jxravity.  hijih  colored- the  typical  .so-called 
fever  urine.  Sennn-all)umin  is  usually  present,  and.  deiiending 
upon  the  amount  of  inflannnator>-  (vdema  into  jilonieruli  and 
tuliuh's.  never  more  than  in  traces.  In  morphotic  elements  this 
urine  is  |M)or.  as  the  proi-ess  never  leads  to  extensive  loss  of 
cellular  elements,  and  the  exudate,  as  we  .saw.  is  purely  serous. 
The  first  indication  of  recoverv'  is  rapid  in -rease  ii  the  amount 
of  urine,  which  indicates  clearing  of  lymphatics  and  cupillar\- 
enjrorfrement ;  with  return  to  physiological  fu-ictions.  alhumin 
(lisap|)ears  and  the  urine  loses  its  increase  in  concentration. 

Closely  allied  to  nephritis  simplex  is  a  ty|)e  which  is 
characterized  not  only  hy  parenchymatous  degeneration  and 
iiitlanunator>-  (edema,  hut  hy  a  marked  de.scjuamation  of 
ei)ithelium  and  excessive  proliferation  of  the  same.  To  this 
subdivision  the  term  nephritis  prolifera  mifiht  proi)eriy  l)e  fiiven 
as  distinfiui-shinji:  it  from  the  simple  form.  It  was  called  by 
\ircho\v  the  catarriial  form  of  nephritis;  later  it  was  much 
nefilected.  Imt  recofrnized  by  Orih-'  and  Kaufnvui-  as  desqua- 
mative and  proliferative  papillar>-  catarrh  on  account  of  its 
predominatinji  appearance  in  the  medulla  t)f  t  he  kidney.  In  this 
form  we  may  squeeze  out,  at  autopsy,  an  alnuidance  of  turbid 


<ll) 


KItli.ll  I 


i>i*i:  \-«K 


fliliil  trniM  llic  iiinlulla.  inii~i>liiii;  <'t  ciiitlicli.il  ct'lls  iiinl  ilctillus. 
It  i«.  lidWi'Nrr.  I)\  llu  liM'.-llls  colltilH'il  to  IIh'sc  Ilililllo.  Iilll  ucfU's 
«litlii>c.  :i>  icct'iil  iiivcsliLL.ilioiis  ••!'  ntlicrs  .irid  iii\  own  li;tvc 
.slidWii;  it  is  x'cii  |i.iHiciil;iil\  in  cases  wlit'ii  tin-  pan'iirlis  iiialuiis 
ilt'ucticratitui  of  llic  fiiitlicliiiiii  is  tiiarl\f(l.  ami  imicii  of  il 
(Icstroxctl  ami  lost.  Il  iiia\.  tiicrcl'on'.  Imtoiiic  assurialcil  willi 
all  tillicr  tvpcs  nf  ncpliiitis.  and  |ila>s,  as  1  pifsc  iitl\  li(»iic  t(» 
show,  iiiucli  inorc  nf  a  nilc  in  tlic  inilaininainn  |ini((s>  tlian 
is  nsualiv  supposed  I'iir.  't  .  Wiiile  \inliM\v  liad  ol)serve<|  the 
desiiuaination  of  tiie  epithelium,  it  was  shown  l>\  Heer  in  1S')1» 
th.it  tliese  <'ells  rapidly  and  excessively  pfolifeiated.  that  the 
tubules  dilate  and  are  fre(|ueiitly  filled  with  these  cell  masses.-' 
lie  rejiardcii  this  h'sion  as  an  inllaminatory  phenomenon. 

Later  ohservers,  like  Weiiiert,-'  (iol^ii,-'  and  others,-"  studied 
these  cell  types  more  carefully  and  descrihed  the  fortnalion  of 
epithelial  uiaiit -cells  in  neiihritis  il"i^.  ()'.  Hut  the  idea  <iained 
^irouiid  that  they  represented  either  true  re<:eneratioiis.  or.  at 
h'ast.  reucnerative  attempts  with  failure.  The  studies  of 
.\rnold -■  and  Mauinirarteii-'Ntn  the  formation  of  tulx'rcles  in  the 
kiilney  coimected  this  proliferation  more  definitely  with  the 
defenses  of  the  tissue  aii:iinst  the  tuherculoiis  invasion.  ;ind  my 
own  studies  in  the  m.itter  have  convinced  m«'-"'that  we  have 
here  liefore  us  a  type  of  parenchymatous  infiaminatoiy  reaction 
analogous  to  the  excessive  epithelial  proliferation  in  certain 
other  infl.-immations;  for  instance,  in  the  luniis.  in  catarrhal 
l)neunionia.  1  was  led  to  this  view  hecause  of  the  predominance 
of  all  irre,^ul;ir  cell  activity  and  .atypical  i-ell  for'!'.:;,  lo  which  we 
<-aimot  attrilmte  any  normal  reslitution  or  norm.al  activity,  the 
formal  ion  of  syncytial  liiaiit -cells,  and  the  exc<ssive  iiitracanalic- 
iilar  proliferation.  The  latest  oliserv.-itioiis  of  lleineke"'  on 
the  kidney  chaiii:es  in  corrosive  >ul>limate  poisoiiinu:  have  hroujiht 
corrohoration  of  this  contention,  for  he  too  oh.served  the  satiie 


llKtiKVKII  All 


\y.     \\l>    lAI  l»\TIVr.    KKMIUKS    t'K    NUrillllTIS  (il 


I  111    "i       Nipliriti-  |iri>lifir.i  il   piii.|iiiliv:i 


pMrtr  (.r  lli'iili'-  liMip-  tillr.|  :in<l  clil;ili;.l 


I,  ii.wlv  fur I  c.  II-.  r.  rii|£iiiz:ilp|c-  l'\  lluir  -\'f.  -Ii;i|h',  picpI(ipl:iMii,  :iiii|  riclilv  (liriilnalir 

■  Il  j       Oiii'  vctv  Imuc  ("iivolilliil  IiiImiIi'  lllli'il  Willi  iHiii.lic  nil  iii;i-!-r>,  :i  -iiiMllcr  niH' 
,\f.      'I'lic  lllliTM  IlillK  liliroll-  li»Mi-  lliirkrIHil  ■    illMI. 


riu.  (>.      f.ii'iiMliMr.  ..f  iiiuiiimii-h-ir  j; 


i;tt:i-fcti  til 


•*>nvr,!iiH-t  iuS-uli' 


I)K<  !;\KI«.\TI\  K    AM)    KXIDATIV  K    KKATl  HKS   OK    NKPHIUTIS  03 


(lilTii-  'xcossivo  opitlu'lial  proliferation.  Theso  cells,  nion'over. 
were  .  tinctly  phiifiocytic  to  the  necrotic  cell  mask's.  In  this 
way  s<'veral  jienerations  of  epithelial  cells  were  produced,  dis- 
iiitejirated.  and  eliniinate<l  Ix'fore  true  |H>rnianent  rejieneration 
commenced.  The  epith(<li:d  proliferation  in  nephritis  is.  then, 
an  inHanunatory  phenomenon,  and  should  Im>  appreciated  as  an 
iiniM)rtant  factor  in  the  pathofienesis  of  the  inflanunation. 

Functionally  the  lesion  lH>comes  evident  hy  the  fnt'  discharjue 
of  the  newly  forme<l  Mid  des(|uamatin<r  cell  masses  and  epithelial 
detritus  in  the  urine.  This,  therefon-,  is  richer  in  niorphotic 
elements.  .Microscopic  e.xamination  shows  the.se  cells  in  a  fnn' 
state,  when  they  are  frecjuently  mistaken  for  leukocytes,  or  in 
the  fonn  of  cellular  or  granular  casts. 

This  leads  din'ctly  to  the  im|M)rtant  and  severe  kidney  in- 
flammations, which  I  ^roup  under  the  cate;!:(»rv  of  nephritis 
dejienerativa  et  exudativa.  .\s  the  name  and  its  adjectives 
imply,  we  include  here  ty|K\s  in  which  either  the  de<renerative  or 
the  exudative  features  |)redominate,  or  in  which  lK)th  appear  so 
inten.se  and  characteristic,  and  lead  to  such  |)ermanent  alterations 
in  the  orjran,  that  (piantitatively  and  (jualitaUvely  they  fjo  far 
U'vond  the  lesions  of  simple  and  proliferative  nephritis. 

It  is  in  these  complicated  forms  of  nephritis  |)articularly  that 
opinions  difTer  widely  as  to  patho>:enesis  an<l  histofjene-sis.  I 
h.'ive  already  sketched  in  the  introductory  lecture  the  funda- 
mental (|U(>stions  which  are  involve<l,  l)Ut  it  is  neces.sarv  here 
that  s«>me  attention  he  paid  at  least  to  the  more  important 
details  of  the  discussion. 

Vou  will  n'lnenjher  from  Miy  first  lecture,  and  from  what  I 
s.iid  in  the  iM'jiinniiifi  to-day,  that  modern  pathologists  are 
divided  into  .si'veral  <-amps  as  it'jiards  the  conception  and 
definition  of  intl.-unni  ition. 

One  jrroup  adheres  to  the  old  term  (»f  parenehymatous  in- 


11! 


CI 


MKKillTS    DISKASK 


fl;iiimi:itiun.  AscliotT,  for  instance,  in  liis  new  hook  on  patlio- 
loiiical  anatomy,  states:  "  As  lonv;  as  cloudy  swellinir  of  the  tu- 
Imlar  epitlieliuni  controls  llie  picture  of  tlie  inilaiinnatory  reac- 
tion witliout  particular  cliaiiiic  in  tlie  vascular  coiuiective  tissue 
and  the  irloinerular  l)odies,  one  is  justilied  to  speak  of  a  tulmlar 
nei)hritis."  The  parenchymatous  deiicneration  is  taken  as  the 
i-esult  <if  an  iiiilanunatory  reaction  and  rcMresents  a  condition  of 
increased  secretion  with  increased  formation  of  j)rotoplasinic 
granules,    colloid    and    fluid    drops,    and    vacuoles.      Ilxudative 

ult 


r(>s 


processes  are  looked  upon  either  as  an  accoinpaiiitnent  or 
of  the  ei)ithelial  irritation. 

This  view  has.  as  you  .see,  a  relation  to  the  old.  previously 
dis'ussed  ide.is  of  Virchow  on  parenchymatous  de<:eneration  and 
inflau'.mation.  Hut  it  ditTers  from  them  essentially  in  rejiardinf;; 
the  parenchym.itous  dejreneration  ;is  an  (irlirr  pro<'e.ss.  the  direct 
result  of  an  injury  which  is  followed,  and  not  caused,  as  Virchow 
would  hav(>  it,  Wy  exudation.  I'an'nchyinatous  infl.Mtnmrtioii  is. 
therefore,  the  prototyp<'  of  .an  iiiHainmation :  only  when  the 
epithelium  is  killed  the  itiflammation  U'comes  modified. 

A  se<'ond  irroup  restricts  the  inflanun.itorv  conception  solely 
to  the  v.iscular  and  exudative  reactive  ehany:es,  anil  divorces  the 
deiicnerative  features  alisohitely  from  them,  'i'hese  latter  may, 
in  the  minds  of  .some,  eitlwr  precede  and  excite  tlie  inflammatory 
chanjres  (.Marchand.  /.  r.  i.  or  they  may  initiate  .and  cause  a 
deirenerative  parenchymatous  involvcjuent . 

Nauwerck  "  has  come  out  p;irticul;.rly  strong:  for  the  Latter 
view  in  ne|ihritis  in  an  attempt  to  disprove  \Vei;rert's  conceptions, 
hut  von  Kahlden  '■  properly  reinarks  th.at  in  an  extensive  study 
he  has  never  met  such  cases. 

.\  thinl  jrrou|).  finally,  holds,  to  (piote  wi.h  l.uharsch.  that 
only  the  comhination  of,  and  intimate  correlation  of,  alterative. 
exu<l:itive.   and   proliferative  chan'res  constitute   inflanun.ation. 


l)K<ii:\Kl<ATIVK    AM)    KXI DATIVK    KKATIKKS   OK    NKPHKITIS  ()0 

Tliis  ;rn»u|)  of  invest iv;at()rs  olinunalcs  «'iitir('ly  from  tlio  iiiHain- 
?iialorv  ('on<'('|)tioii  the  (Ic^rciicrativc  parcnchyniatoii.s  processrs, 
and  (Iocs  not,  tlicrcforc.  tolcrat*'  the  so-called  parencliyniatous 
inflanunations  of  the  older  writers.  It  rejects,  for  instance, 
entirely  the  term  of  parenchymatous  myocarditis,  neuritis, 
myelitis,  :in<l  so  forth.  It  denies  the  inflanunatory  character  to 
purely  nutritive  and  alterative  chan«:es  in  the  parenchyma, 
unless  coml)ined  with  exudative  and  proliferative  changes. 

It  is  this  firoup  of  invest ii^a tors  which  would  separate,  in  the 
case  of  the  kidney,  as  we  saw  in  th«>  lK';>innin}i  of  this  lecture,  a 
non-inflanunatory  |)arenchymatous  de<re!ierati(>n  as  an  e.s.sential, 
l)ul  no*  a  nephritic,  lesion. 

(hie  c.iii  recojrnize,  therefore,  various  ;itt<'mpts  of  classifica- 
tion on  the  part  of  invest ijiators: 

I.  Degenerative  chan<:es  in  the  parenchyma  form  the 
<'s.sential  feature  of  nephritis;    and  they  may  or  may  not    l)e 


.iccompamed  or  tollowed  hy  va.scular  exudation. 

2.  N'a.scular  exudation  is  the  characteristic  phenomenon  of  a 
nephritis:  i^n  This  may  or  may  not  become  associated  with 
dey:enerative  chaiifics  in  the  parenchyma.  (/*)  It  de|M'nds  uj on 
the  parenchymatous  destnK'tion.  id  It  may  involve  the  whole 
v.iscular  apparatus  of  the  kidney  or  only  parts  of  it  ifjlomerulo- 
nephritis). 

;{.  .\11  estahlishe<l  inflammatory  affections  of  the  kidney  are 
diffuse;  that  is,  they  involve  all  the  structures  (parenchvmatous 
and  vascular!  of  the  or^aii,  althouv:h  they  may  1k'  unevenly 
distriliuied.  .\n  ;ilt.s<>lute  de|M>ndence  of  one  change  upon  the 
<ither  c.mnot  Ik'  ma<le  out,  although  at  the  i)e^imiinf:  either 
dejienerative  or  exudative  features  of  the  proc<>ss  m;iy  a|)|H'ar 
more  prominent,  and  in  a  numlwr  of  ca.s<'s  may  contimie  so. 

This  latter  standjxtuit  ap|H'ars  to  me  the  most  acceptable  one, 
with  the  followiti^;  (jualitications: 


m 


MKK.IITS    DlSKASi; 


1.1  •    The  term  iiifl;imm;ili<»ii  (•(•inprisfs  tlicsimi  toljil  of  lliosc 
onclMlcd  I'lil   iKii  ;il)S(iliil('ly  (Icih'ikIciiI  dciicm-nilivc.  piolifci- 


Mlivi'.  Mild  «'\iid:ilivt'  ( 


Iwiniics  which  ;irc  llir  (hrcit  rrsiih  <if  mii 


injiirN  t(i  M  pint.  I'urc  dc^ciicnilivc  :iiid  inohfcnitivc,  ;is  well  :is 
\m\v  cMuhitive.  iiitl.iiiiiii.ilions  do  not  exist,  .dthoiiuli.  for  re!is<iiis 
In  lie  discussed  l;iter.  one  of  tliese  iiifl;iliiiii;itorv  ;it t lilnitcs  m;iy 
liecniiie  iiuich  more  proiioiiiiced  ;iiid  piomiiieiit  th.iii  the  others. 
/)'  A  conliiieiiieiit  of  Mil  iiillMiniiiMtoiv  lesion  t<i  m  pMilicwlMr 
port  loll  of  the  kidney  siilislMiice  for  eXMiiiple.  iiloinenin  does 
t  exisi.  so  th.il  tiie  term  i:loiiieriiloiieplintis  is  wroniily  iise<l  in 
h  .1  s«'iise.  ( )ii  the  other  hMiid.  altliou«ih  there  is  no  kichiey  in- 
liich  uloiiienilMr  chMiiycs  mic  hickinj:.  yet  there 


no 
SIK 


MiiiniMtion  III  \v 


is  no 


proof  tliMt  tliis  lesion  is  the  stMrtinu-poinl   of  m11  cmscs  of 
nephritis. 

('  1  therefore  include  the  dejicnerMtive  feMlures  ms  inflaiii- 
niMtorv  idieiioiiu'iiM.  Miid  reuMi'd  them  ms  evideiiv-es  of  mii  injury, 
or  the  pMssive  feMtures  of  mii  inflMniiiiMlion.  cotitra.sled  with  the 
pidlifer.itive  Miid  exuiLitive  rcMclive  phenonieiiM  of  the  |)roeess. 
Hut  the  close  MSsociMtion  :ilid  lel.itioii  hetween  the  pMS.sive 
deuciieiMlive  Mild  icMctive  prolifeiMlive  pMieiichymMlous  mikI 
exudMtive  diMiiucs  niMke  it  impossilde  in  my  mind  to  ever  sep- 
MiMte  them,  the  one  ms  non-infl;imiiiMtoiy.  the  other  ms  inllMmiiiM- 
torv.  Pure  pMrenchyiiiatous  devieiierative  lesions,  iiiiMecoin- 
pMiiied  \>\  Mt  IcMst  Mil  inflMmiiiMtory  (I'detiiM  of  the  parts,  do  not 
exist.  Mild  it  is  .in  MitificiMJ  stretchinu  of  idcMs  to  keep  them 
distinct  from  the  conceptions  of  the  iiitlMmiiiMlory  process. 
This  conception  of  inflMmm.ition  is,  therefore,  not  tlwit  of  ;i  sin«rle 


either   purely   jKissive    (\'ircliowi   or   purely    iCMctive    i  moder 


III 


process,  hut  Mil  expression  of  the  sum  totiil  of  <i('iieticMlly  related, 
partly  injurious  and  partly  helpful.  proces,s(>s,  which  are  excited 


li 


V  irritants. 


'(' |.:iri 


ZhkI'i.  I  •I"'  'I' 


II    U('jirliW;ir(lKrri 


Stiiiid  ilir  I.1I1 


III  ilir  KiitzuMiliiiiii, 


DfiiiMlir  Kliiiik,  \i 


l)K(iK\KU.\TIVK    AM)    KXIDATU  K    KKATIKKS    OK    .NKi'llKITIS  (i7 

Other  coiici'ptioiis  suffer,  in  my  ((pitiion.  from  the  inherent 
weakness  and  artificiality  of  too  strict  classification. 

Following  the  ori;rinal  description  hy  F\lel)s  of  glomerulo- 
nephritis, it  has  l)e<'n  the  effort  of  many  to  estaldi.sh  this  as  a 
((articular  characteristic  ty|M'  of  nephritis,  and  s<mie.  like 
I'riedliinder  ■'  and  Xauwerck,  have  ;:one  so  far  as  to  s|M'ak  <»f 
glomerulonephritis  only  then,  when  the  jil<">i<'nili  alone  are 
atTected.  aixl  in  a  characteristic  inflammatory  thrombosis  of  the 
capill.ary  tuft. 

On  tile  other  hand.  IJiMiert  "  regards  glomerulonephritis 
as  the  start in;r-point  of  any  nephritis,  and  he  therefore  cla.ssifies 
any  further  chanjies  as  suhdivisions  of  this  uniformly  |)rimary 
•  inatomical  lesion.  While  he  strictly  adheres  to  a  division  of 
pai-enchymatous  ;ind  interstitial  nephritis,  lie  interprets  them 
as  sulxlivisions  of  the  jilomerular  afTection. 

These  represj-nt  rather  extreme  views,  and  in  my  opinion 
suffer  from  the  endeavor  to  create  ty|H's  of  nephritis  either  out 
of  st.ijies  of  a  lesicni.  or  from  an  undue  imj)re.s.sion  witli  pniminent 
I'e.itures  of  the  inflammatory  [irocess  in  certain  cases. 

Dejretierat ive  and  exudative  nephrites  are  always  tiie  result 
of  inten.se  >:eneial  and  characteristic  intoxications  and  infec- 
tions; al)ove  all,  the  acute  exanthemata,  particularly  durin;:  the 
Lite  stajres  of  xarlet  fever,  hut  other  infectious  di.sea.ses  as  well, 
furnish  a  larjre  numU'r  of  the  ca.s<>s  the  .severe  s<'ptic  condi- 
tion of  the  usu.al  or  s|H'cific  tyjM's.  .se|)tica'mia,  pya'mia.  pneu- 
monia itlie  latter  not  at  all  infnMjuently i,  syphilis,  erysijK'las, 
and  others.  Sometimes  the  primary  focus  of  infection  may  he 
dillicult  to  detect,  or  may  ap[H>ar  insijrnificant,  as  in  an^rina 
pharynjiis.  tonsillitis,  or  purulent  otitis.  But  there  can  l)o  no 
doubt  that  .stnere  nepliritis  may  Ih'  either  asso('iate<l  with  or 
follow  the.se  apparently  trivial  infections.  The  mouth  and  ear 
should  tlu'refore  always  Ik>  ins|M'cted  durinji  life  and  at  autopsy. 


II 


i  la 
III 


('»S 


HKKillT  S    DISIASi; 


(Irosslv  the  kidiifv  shows  llic  ciiiulitioiis  of  simple  iicpliritis 


intt'ii 


silicd.     It    is  l:ii-; 


:cr 


than   iiorinal.   firm,   Iml-riiiy;.  and  tin- 


surface  |)idmiiH'litl\    roiivt 


\V!tl 


leaves 


>moolli 


\.      The  capsule  stretched,  remove*! 
surface,  with   an   opaijue.   dusky. 


ie( 


Idish-while    iirouml-coliM.    and    lumierous    irre^iular.    small. 
|M.inl-like   or   streaky    hemorrhaues.      These    may    occasionally 
(lit 


ume  such  (luueiisioiis  as 


to  ^.ive  to  the  whole  kidney  a  pre- 
(hwninaliniily  liemorrh.i^ic  apiH'anmce.  Sometimes  small  areas 
of  yellow  fatty  color  .are  irre-rularly  distriliuted  il'itr.  T'.  On 
section  the  kidney  is  juicy,  and  discharj:es  readily  a  turhid. 
leiienialous  lluid.  The  cortex  is  enormously  swollen,  pale,  and 
contains  irrejiular  lu-morrhai:i<-  streaks  and  dots.  The  normal 
^lom-rular  rows  have  apparently,  to  yireat  extent.  disapjH'ared. 

lent   in  the  form  of  .iilistenin<:.  white. 


es. 


'11 


le  mterveinnji 


hut  the  i:lomeruli  are  evi< 
sliditly  elevated  |M)ints  or  mimite  -irami! 
tuliular  suhstance  appears  thick  and  cloudy.  The  line  of  de- 
marcation Letween  cortex  and  m< dulla  is  uiuisually  well  marked. 
I.v 


a   mo 


re  prominent   hut  ditTuse  piiikish-}:ray   cyaiiotici  ap- 
|M'arani'e  of  the  me<hillary  portion.     Here  also  a  j:rayish  swelliiiji 


with  oliliter.ition  of  tin-  norma 


1  ra\s  is  marked.     These  are  the 


evKlencc; 


.f     tl 


le    wellH's 


tal>lished    forms;  and     n.iturally    th(> 


variations  lu.-iv 


lesion;  secon* 


U'jrreat.     These  de|K'nd.  first,  on  the  stajic  of  tin' 
llv.  on    the  (|ualitative  features,  dejicnerative    or 


vascular  cliaiii:es  predominating. 


In  tl 


le  ea 


rlv  st.ijies  the  evi- 


dences of  inflammatory  hypenemia  are  much  more  prominent 
thanlater.wheiide'ienerativeand  part  icularlye\udativ<<  chan«:('s. 
by  mechanical  c(»iiipression.  a;r;;re<:ation  of  necrotic  material, 
and  hv  the  general  (edematous  iml>il)ition  of  the  part.s.  chanjie 

)r  vellowish  J)ale.  and  make  the 


the  picture  from  red  to  ^ray 


mar 


kin 


":s  trra* 


luallv 


UK 


listinct.  and  cause  finally  entire  olilitera- 


tion 


lie  7  Xi'pliriiis  ili'^mirraliva  rxiiilativii  li:rm(irrlijmicii,  frmii  lii-i'  (if  iiulniarilitis 
~'  f'lr.i  A  hiT>:<\  Imlt'ilii;,  uiiil'ormly  --wnlliii  kuliiiy.  All  iKiriiial  iiiiirklii/is  li>M  llrni;.r 
i:i!i>ii  Uiw.i  II  iiii'iliilhi  uiiil  n)rt<'\  olililiTUtid.  Smaller  innl  liirci  i  liiiii,irrlijM;i!.  iiiicvihly 
liii  uiiifcirmly  ilislrilmliMl  iivir  tin-  hIihIc  kiiliirv  iiirt<\.  liil(T|Kila!.  i|  iiir  sinirluri'lt  ^^ 
yi  l|ii\>i^li-w!iiti'  Mnviks  ami  iialdus  wliirli  <iirri-!.|Kinil  td  iMnlmiM  iiri<l  •hfri  ii.nitivi' 
laily    alius       Tin-  nll.Tliil  ca|iMili'  <i-il('tilul'iu>,  ViHnU  iiijcctcil       \\(i>;hl,   tlMt  mil-. 


l»K<iK\KH.\TIVK    AM)    KXI DATH  K    KKATI  UKs   UK    NKI'IIHITIS  (»U 


I  ili.  s  M:irkr<|  rloiidy  nurllintt  ami  HcroiiA  iiiiliiliilicili  iif  Kliiiiirriihir  i':i|>illai'ii'>,  Irtiil- 
1  111;  Id  fusiiiii  ami  liyalinr  >\H'lliii(j<'f  tlir  liilmlo:  miiiic  imrt'asr  in  iiiiiiilx'r  ami  «izi'  of  cmli*- 
llnlial  nurlri  Scrims  fvililalr  ililci  caiisular  -paiT,  IcacliiiK  t<>  ililataliiin  ami  In  liyillim- 
-wrIliiiK  of  tiji'  i'a|>-'iilar  i'|>illirliiiMi.  wliiili  is  icraililally  liftnl  olT  llii- liasciiit'iit  iiiriiiliriuiir 
111  I  pil-liril  lowar.l  llic  lili'l.      I'i'W  Irukoryti-s  in  tlii'  rapiular  spare.      X  -•><). 


lii!.   '^-    Tiifl    of   jslomcriiliis    with  ilisliiiil   scparalioii   iiiio  lolmli's;  inlraiapsiilai  I'xmla- 

liirti  more  inarki'il         •    '-'•>•(. 


It 


ill 


111 


lid  10  V.iriiiil«  itUiMii'ruliir.  iMriiiloiiifnihir.  tiiliiiliir.  :iii<l  |i<Tiliil>iil:ir  ih.iliK"*  >» 
iii|iliiilj-  i\i|i|:itiMi  il  iliitiiKrMliv.i.  |«irtlv  niiri-^i'iili',!  in  I'in'.  s  :iiiil  '■>  In  iiilditiiin. 
ulniiitriili  »iili  iiiurkcij  itiini-  an<l  |M'nr!ii»iil:ir  i'MhIiiIi'.  uilli  iii-ciii-i»  uf  nnr  ulunirnilii-: 
:iMiilliii  liN.iliiir  l';il<liy  rflliil.ir  lAiiilali'  ill  |M'ri(ilmniTiiliir  :iiiil  iiilcrnilniliir  li-»iii- 
rnliiilt-  III  \an<iii»  li>riii«  "f  iMiirinliyiii.iliiiH  ilcui-iii'nilinii  iinil  miTiisi!.  In  llir  ii|)|mi 
|i;lll   111    I  111'  llirtliri'  tllhlllr-  llmv   Ic  »ll'll  In  rii|lt;iill  li  llki"Mf«         ■     tj."i 


I'iu    II       III  till'  iipiwT  piirl  iif  till-  ficlil  a  dlomrriiliis  slio«>  M'piinitiiin  inln  <li«liiui 

l.il.iilo  liv  fu>iiiii  iif  caiiilliiry  liMips.  willi  lucalizi'l  alliicli nl  loraiisulc.      A  (jIohhtiiIus 

li.li.tt  ilii-  allows  niiiipioMiiii  l>y  fXiiilalr  anil  liyaliiic  Iraiisfiiri.ialiiiii  of  llir  liifl.    JHiirkrii- 
iiiK  (if  niniiiTlivc  ll.-wiir.     ( "yslir  liilalaliiin  of  fiilmir  in  lower  part  of  lirlil.       ■    I7"i. 

71 


MICROCOPY    DESOIUTION    TEST   CHART 

ANSI  and  ISO  TEST  CHART  No    2| 


^  '^PPUEDJM^IGEJ 

^^1  'f-^-^    f'^S)    M-J.n    St'Mt 

S'-S  "ri^rf^'f;   '^'*   ""''''  '*^09        USA 

rjse  ,  '  1  6)    ♦8J  -   0300  -  P»ione 


DE(;i;\KHATIVK    AM)    KXIDATIVK    FF.ATIHKS   OK    NKI'HIMTIS   73 


I'in  \2  I'lisioii  of  (jlonicnilar  tuft  liy  ((iinprcssion  of  ('xiidittc,  wliicli  leads  to  its  iio- 
(■ii>sis,  and  also  ilihiti's  the  capsule.  Beloxs  it,  hyaline  (colloid)  cast  in  a  tubuh'.  I'cri- 
nloniiTular  airl  p<rilul>ular  cellular  infiltration.       '    JIH). 


Kin.  IM.  -  l{ielily  cellular  (leukocytic)  exudate  into  (cloineriihir  capsule,  with  ilisintL>Kr»- 
tion  of  the  glomerulus.  Similar  exudation  in  surroundin)?  ti.ssue  and  into  the  tubules, 
which  show  parenchymatous  swelling.      X  210. 


DKU i:\KKATIVK    AM)    KXIDATIVK    FKATIKKS    OF    .NKPHKITIS   75 


FiK,  14- — Typical  capsular  ppitlidial  proliferation  in  Klomcruli.  becoming  unulually 
flattcncil  and  fibrillar,  willi  markoil  fusion  of  capillaries,  leailinn  to  separation  of  Blotiierular 
lobu^w  anil  final  ilisintegration.     X  1S5. 


I 


I)K(iK.\KHATI\  K    AM)    KXIDATIVK    KKATl  l{KS    (»K    NKl'IIHITIS   77 


Kilt  l"i.  MMikil  punilciil  inlilinilioii  ami  sliiptiylococcal  i'iiil)oli  in  the  (jldincnihir 
loopx,  whii-li  has  cxli'iiclcd  to  tlic  pcritfloiiicnilar  lissiic,  Icailintj  to  necrosis  of  tlic  «)iolr 
glomerulus.     The  sinrriuiiiliiiu  luliulis  sliow  typical  paiciicliviuatoiis  ilcdcnrration.     X   1">(). 


1 


I'iK    10. — ("oiiiplctc  piirtilciit  necrosis  of  glomeruli.     Capsular  space  and  tulmle 

free.     X  2(K). 


relatively 


DKdK.NKIiATIVK    AM)    KM  DATIVK    KKATIUKS    (»K    NKI'IIUITIS   71) 


liK.  Hi.r  lii|)injr:i|)lii(:il  piiliirc  (if  nephritis  rxM(l.iliv;i  ili'({ciicr;itiv;i  li:iiii()trliii|jl(M. 
In  the  ii|i|.(r  piiii  of  field  seviTal  (jloineriili  ill  stall-  of  necrosis.  Cellular  inlilliation  of 
interstitial  tissue,  I'areticliyniatoiis  ileiieiic'ialioti  ami  nernisis  of  epithelial  cells  of  eoii- 
voliiled  tiiliules.  with  iiiarkel  lieniorrliaKic  exudate  into  them;    (itie  hvalitie  cast.      X    Iti'J 


i 


Tits.  17.— lleniorrhaKie  necrosis  of  a  gloinenilus.     N'porolie  infliimmatorv  cells  siirroiind  the 
Kloinoruliis.     IlenioiTliaKic  exudate  into  tiilmles.      x  I2">. 


DKCKNKUATIVK    AM)    KXl  DATIVK    KKATIHKS   oK    XKI'HHITIS  SI 


I'ilJ.  IS.— Inflaiiiniatorv  cxinlalioii,  fusion,  and  necrosis  of  gloiiiiTiilar  tuft,  with  u'dpiimtou.s 
swi-lliuK  of  <'apsular  cpitlicliuni. 


l>KliK\i;U\TIVK    AM)    KXIDATIVK    KKVTIHHs    oK    VKI'MUITIs  ,S;t 


I'itJ    l!l.      lltiiKiriliaKic'  fiisiim  aii'l  ii.'crosis  of  liifl.     Tlir  siirfiKT  still  shows  f.-w  dropsiciil, 
swolliii.  iMiilotlu'lul  or  cpilliclial  (clIs,     (Kilrtiiatoiis  swclliiiK  "f  capsular  cpitlicliiiin. 


iiMi 


DECENERATIVE   AND   EXUDATIVE    FEATURES   OF    NEPHRITIS  85 

In  certain  cases  hemorrhajies  occur  early  and  persistently, 
and  therefore  jiive  to  the  whole  lesion  a  characteristic  appearance. 
For  the  sake  of  study,  we  may  divide  the  manifold  microscopic 
processes  under  the  following?  headings :  chanjjes  in  the  glomeruli, 
changes  in  the  tubular  substances,  changes  in  the  intertubular 
substance. 

First,  the  changes  in  the  glomeruli  have  been  well  studied 
and  are  of  the  greatest  importance,  for,  as  we  will  see  later,  the 
ultimate  fate  of  the  kidney  depends  largely  upon  them. 

The  first  changes  'w  the  glomeruli  are  degenerative  in  char- 
acter and  affect  the  endothelium  of  the  capillaries  and  the  lining 
epithelium  of  the  tuft.  Coincident  is  inflammatory'  hypera'mia 
of  the  capillaries,  rapidly  followed  by  serous  imbibition  of  all  the 
structures  of  the  tuft.  In  severe  cases  all  of  these  are  well 
accentuated  from  the  start.  In  milder  cases,  von  Kahlden-*' 
found  degenerative  features  the  very  first  phenomenon,  con- 
sisting mainly  of  fatty  degeneration  of  the  capsular  epithelium 
and  capillarA'  endothelium.  Even  in  these  milder  cases,  how- 
ever, infiammator>'  a'dema  into  the  tuft  and  into  the  space  be- 
tween it  and  the  capsule  follows  so  rapidly  that  it  cannot  well  be 
separated  from  the  degenerative  changes.  As  the  result  of  lx)th 
of  these  degeneration  and  serous  exudate — the  capsular  epi- 
thelium is  lifted  off  the  basement  membrane  and  pushed  forward, 
the  epithelial  cells  of  the  tuft  loosen  and  desquamate,  hyaline 
swelling,  leading  to  thickening  and  turbidity  of  the  capillarj' 
walls,  occurs.  As  a  result  of  this,  fusion  of  the  lobules  follows 
with  the  characteristic  inflammatory'  accumulation  of  leu- 
kocytes, and  their  emigration  into  the  tuft  and  capsule. 
The  appearance  of  free  red  cells  is  frequent.  The  exudate  lies 
partly  in  and  between  the  convoluted  loops  and  lobules  of  the 
capillaries,  but  later  fills  the  capsule,  gradually  compressing  the 
convoluted  tuft  toward  a  peripheral  portion  of  the  capsule.     As 


:=-.=        * 


S() 


HHKillT  S    DISKASK 


a  coiisccnuMicc'.  the  tiifl.  thus  affected,  appears  primarily  larj^e, 
plump,  pale,  filliuji  the  capsule  (•()m|)letely:  hut  later  the  capsule 
distends,  as  the  result  (if  pressure  from  coajiulated  exuded  masses 
and  cell  detritus,  .and  leaves  the  capillaries  retracted  and  less 
conspicuous  I  Fins.  S  to  V2k 

Much  discussion  has  arisen  over  the  (|uestion  as  to  whether 
here  proliferation  of  the  epithelium  lininj;  the  tuft  occurs.  On 
account  of  th(>complicated  pictures  in  the  tuft,  it  offers  particu- 
lar difliculty. 

I  do  not  share  the  view  that  this  takes  j)lace  to  any  extent, 
llvidently.  the  initi.tl  dejr(>nerative  chanires  and  the  other  inflam- 
matory conditions  make  this  impossible.  The  hulk  of  the  nuclear 
increase  within  the  tuft  appears  to  me  of  leukocytic  and  en- 
dothelial derivation  iFiii.  \'Ak  On  the  other  hand,  proliferation 
of  (he  epithelium  of  the  capsule  is  a  freipient.  rather  constant 
|)heiiomenon.  It  is  seen  particularly  heautifully  in  scarlet  fever, 
and  .sometimes  in  the  other  exanthemata,  .spvei'e  septic  condi- 
tions, al.-io  in  syphilis.  Whether  it  is  a  very  oiirW  phenomenon 
is  (loul>tful,  \'on  Kahlden  was  never  ahle  to  observe  it  in 
very  recent  cases.  It  is  certain  that  it  occurs  only  in  well 
establishe(l  nephrite-;.  One  can  oh.s(>rv(>  th.at  jiradually  rows  of 
l.ariic  epithelial  or  epithelioid  cells,  followinii  the  inner  circular 
wall  of  the  capsule,  concentrically  advance  from  the  periphery 
toward  the  lumen.  This  proliferation  usually  commences  in 
those  lilomeruli  which  have  become  widely  stretched  and  dilated 
by  free  exudate,  .and  in  which  the  tuft  h:is  been  pushed  tow.ard 
one  pole  >  !•  iii.  14 1. 

From  the  opposite  diicction,  this  epithelium  advances  into 
the  capsule,  inclosinii  the  exu(l(>(l  masses  within  it.  and  fifadually 
assumes  a  characteristic  i)rominent  crescent  shape,  which  the 
(lerman  patholojiists  have  lontt  descrilu'd  under  the  name  of 
"  Halhmond"    icrescenti    pictures.      In   some   cases   it    becomes 


DKCKMilJATIVK    AM)    KXIDATIVK    KKATfHKS    OK    NKI'HHITIS  87 


Via.  21). — ('i)inpl('t('  Kraniilar  niMTDsis  of  (jloiiicrular  tuft,  surrimiulcil  l>y  (•"adulated  serous 
exudate.      I'cw  swollen  epitlielial  or  eiidottielial  eells  still  visible.      X  4(H). 


I''i»!.  '21. — Destruetivi'  pareneliymatous  deneueratioti  of  fibular  epithelium.      Fusion   of 
granular  rellular  detritus  into  easts  within  dilated  tubules.      X  H'M. 


DE(}K.\KRATIVE    AM)    KXl  UATIVK    KKATIKKS   OF    NEPHRITIS  89 


£.^" 


rifi    22. — IIIkIi  iiiii|{>>>i><"»><>>>  of  :'  ttlhulc,  with  K>°anular  ('ytoplusiiiic  (lisinlcfcnition  uiid 

iiiK'Iciir  Idss. 


'  ii 


DKiJKNKKATIVK    AM)    K.M  HATIVK    FKATl  HKS   OK    NKI'HUITIS  91 


^■^  ;T£";ci5» 

'iQm 

•     "Til 

1 

Mi 

if 

k 

^-1 

1  IV  ^ 

^0   i-^v" 

I'iK-  2:i.  ( Iniimliir  cfUiilar  llKl^s<•^^.  leukocytes,  iiiid  epillielial  cells  in  tuli\iles,  willi 
extensive  neiTosis  of  these  iles(|ii:iinateil  cells,  infliininialiiry  cMKorRenient  ,'a>'J  liemorrliages 
of  inlcrtulmlar  tissue,      x  22.">. 


I'lK-  -l- — One  tutnilo  with  leukocytic  exudate,  another  with  epithelial  necrotic  iniisses,  two 
others  with  hvaline  formation  in  tubules. 


DKOKNKRATIVK   AXI)    EXtDATlVK    KKATIRES   OK   NEPHRITIS  93 

rxcpHsivp,  replaces  the  whole  of  the  tuft,  and  underjtoes  hyaline 
defeneration.  This  epithelial  proliferation  ap|)earH  to  l)e  an 
inflanmiator>'  phenomenon,  excited  here,  as  in  the  tubules,  by 
the  accunmlation  of  necrotic  and  exuded  masses,  and  fulfils 
primarily  phanocytic-dearinji  duty,  inaujiuratinjj;  fibrous  and 
hyaline  replacement.     These  we  will  consider  later. 

Of  rarer  occurrence  are  the  formation  of  inflammator>- 
hyaline  thrombi  in  the  capillaries,  descril)ed  by  Friedlander;  and 
Hibl)ert  observed  flattening  of  the  thickened  lining  epithelium, 
thereby  adding  to  a  compression  and  impermeal)ility  of  the 
vessels  already  established  by  exudate  and  desquamated  en- 
dothelial cells.  Diapedesis  of  red  blood-cells  may  become  very 
marked,  with  severe  hemorrhages,  complicating  exudation  into 
the  tuft  or  capsule.  In  these,  rapid  necrosis  is  the  termination. 
When  the  exudate  becomes  purulent,  the  glomerulus  meets  the 
.same  fate  (Figs.  15  to  20). 

Secondly,  as  regards  changes  in  the  tubules.  These  are  un- 
evenly distributed,  usually  more  intense  in  the  first  convoluted 
portion,  and  relatively  less  in  the  limbs  of  Henle  and  the  collecting 
tubules.  Senator  '■'''  has  pointed  out  that  this  is  probably  the  re- 
sult of  the  greater  concentration  of  the  blood-current,  after  leav- 
ing the  glomerulus,  which  necessarily  exposes  the  epithelium  of 
the  convoluted  tubules  to  direct  and  greater  injur}-.  On  the 
other  hand,  the  experimental  investigations  of  Lyon  ^"  have  dem- 
onstrated that  in  certain  acute  intoxications  the  ascending  limb 
of  Henle  suffers  most  severely.  They  are  the  least  resistant  parts, 
and  show  disintegrative  and  necrotic  changes  more  commonly 
than  elsewhere.  The  cells,  in  thus  affected  parts,  show  intense 
parenchymatous  degeneration,  leading  to  fatty  degeneration  and 
necrosis.  Unlike  simple  nephritis,  the  tendency  is  here  to  de- 
struction and  loss  of  cells.  Swelling  and  turbidity,  with  loss  of 
cellular  outline,  are  here  marked  from  the  lieginning,  cell  masses 


5>4 


MHKillT  s    DISKXSK 


fuse,  the  prdlopl.isiii  disiiili'jrratcs  «'iilin'ly,  mikI  fatty  siilistaiiccs 
tend  tDMpiM-ar  in  the  foriiiof  fiiH-  dniplcts;  vaniolcs  appear;  the 
laiuc  mamilcs  of  the  cfll,  l>y  (•(iiifiiicnrc.  form  iiccnttic  massrs, 
and  after  lireakiiiii  of  the  cell  inemliraiie,  the  iletritiis  is  dis- 
eharued  into  the  hiinen  of  the  tuli\iles  i  I'ius.  L'l  to  124'.  In 
severe  cases  tlie  lining  nieinlirane  may  lie  eoinpletely  des(|iia- 
maled  I"ii;.  JS  .  It  is  interest  inn  to  note,  and  was  first  |)oiiited  out 
liy  nililtert.  tliat  tlie  ap|M'aranee  of  fatly  substances  commences 
early  and  primarily  in  the  cells  of  the  loops  of  llenle,  aiid  if  we 
look  at  such  a  specimen,  one  cannot  help  lieinj;  astonished  at  this 
ap|»arent  selective  location.  Later,  however,  all  tlie  cells  under- 
-id  the  s.ime  f:ite.  (  h.-iiijics  in  the  nuclei  appear  later,  hut  .ire 
here  of  e(|ual  .severity,  leadiiiii  to  their  entire  lo.ss.  They  are 
destroyed  either  \>y  rapid  chromatolysis,  with  some  persistence 
of  the  achromatic  siihstance.  or  the  chromatin  ix'comes  clum|M'd. 
solid,  and  homoiiciieous.  .so  that  the  ori<iin;il  structure  of  the 
nucleus  is  entirely  losl.  This  condition  is  known  as  pyknosis, 
and  eventu;illy  results  in  iireakinji  up  into  smaller  chromatic 
ni.is.ses  and  eventual  loss.  Finally,  nuclei  may  disappear  Ity  a 
primary  peripheral  disiilaceinent  of  the  normal  chromatin  ma.s.ses 
in  the  i.'icleus,  leavinii  its  body  pale.  Tlie.se  chromatin  masses 
are  later  ('•-^chariied  into  the  protopI;ism  of  the  cell,  where  they 
irradually  disappear. 

Proliferation  of  the  epithelium  is  here  a  characteristic  and 
important  phenomenon.  It  is  excessive,  and  lioes  hand  in  hand 
with  the  necrosis  of  the  epithelium  and  the  accunuilation  of  in- 
flamm.'itory  detritus. 

For  this  reason  it  apj)ears  usually  more  pro!Jiinent  in  the 
lower  portion  of  the  tubules,  where  much  of  the  debris,  on  its 
removal.  sta;rnates;  less  .so  in  the  upper  parts,  but  m;iy  assume 
there  as  "-reat  dimensions,  if  the  necrosis  of  the  cells  and  the 
accumulation  of  inflanunatory  detritus  assume  any  proportion 


DKCiKNKHATIVK    AM)    KXIDATIVK    KKATJUKS   OK    NKI'HKITIS  95 


I 


I 


-t  'iilll|i|(l((|r'>i|ii:iMl:lll.Mi  iil'  ipil  liclilllli  iil  rilliiilcs,  willl  |£l\ilml:il  ((illliul.s  III  lllllK'll 
ol  lillilll(«.        .     t(N) 


Ki(t.  '-<•• — Mjirknl  dilatation  and  distention  of  tul)iilw.      X  12'). 


UMiKNKKATIVK    AM.    KXI  I.ATIVK    KKATI  UKs   OK    \KI-H«ITIS  97 


K'lrut  ihtiil       Nimcof  Ihcrp    hrliiliii  piK iilr<l        <    MNI. 


1  itJ.  JS.    -Ilyalii...  a.i.l  inor.>  soli.l  ,„ll„i,|  ,.,,ms  i„  mhuU-s.    Tlmsr  .(.MlaininK  th,-  ,asts  will. 


i)K(;k.\ki{ativk  and  kxidativk  fkatires  ok  xkphritis  99 

(Fijis.  2;i  and  24).  This  important  fact  appears  plain  from  the 
ol)sorvati()ns  of  Lyon.  Hoineko,  and  my  own.  The  cells  thus  de- 
rived from  the  linino;  epithelium  of  ti.e  tulniles  differ  entirely  from 
the  normal  in  appearance  and  function.  In  the  lower  portion  of 
the  tubule  they  are  <j;efierally  small.  cul)oidal  in  nature,  firowinj-- 
diffusely  within  the  tubules;  in  the  convoluted  parts  they  are 
nujch  larjier,  frequently  formin<!;  multinuclear  <iiant-cells  by 
fusion  or  over«>r()wth.  As  I  said  before,  their  function  must  be 
brou<-ht  into  relation  to  the  inflammatory  defenses  of  the  tissue. 
This  is  indicated,  not  only  by  their  distinct  morpholo<:y  and 
abundance  of  production,  but  also  by  the  phajjocytic  power 
of  these  cells.  Rejieneration  of  typical  permanent  epithelium 
does  not  occur  until  all  inflammatory  irritants  and  products  have 
thus  l)een  removed,  but  then  with  fireat  activity.  The  process 
here  outlined  cannot  but  arouse  one's  «ireat  interest  and  astonish- 
ment from  a  «>;eneral  patholojjical  standpoi»it.  Consider  for  a 
moment  that  hijrhly  differentiated  epithelial  cells,  under  the 
necessity  of  foreif-n  invasion,  so  to  speak,  throw  aside  their 
hi^dier  attributes,  and  produce  an  offsprin<i  which,  not  only 
morpholofiically,  but  also  functionally,  is  distinct.  This  pro- 
duction is  continued,  as  necessity  refjuires,  over  and  over  ajiain, 
until  after  a  time  the  cells  either  succumb  or  liave  succeeded  in 
removinj:  the  cause  of  their  distress.  Then,  as  a  more  wonderful 
phenomenon,  they  are  able  to  reproduce  their  own  orijjinal  kind; 
return,  in  other  words,  to  their  former  morpholojrical  and  func- 
tional differentiation.  In  this  process  are  concealed  from  us 
some  of  the  most  important  and  fundamental  biolo^-ical  laws. 
If  we  were  able  to  follow  it,  we  would  know  what  determines 
proliferation  of  cells,  wh.it  determines  the  functional  differentia- 
tion, and  how  some  proj)erties  may  remain  potential,  to  re- 
develop luider  favorable  conditions.  It  would  l)e  the  greatest 
step  toward  the  solution  of  tumor  growth.     I  will  refrain,  how- 


KM) 


HlUiJUT  S    DlSKASi: 


ever,  from  lioiiii:  into  tlicorctii-Ml  discussions  hove  ;iii(l  return  to 

fiiCtS. 

The  lumen  of  the  tul>ules  contains  more  than  tliis  material: 
leukocytes,  red  cells,  coaiiulated  .alhuminous  exudat(>  enter 
|)artlv  throuiih  their  own  injured  walls,  and  to  some  extent  are 
washetldown  from  the  iilomenili.  Asa  coiise(|uence.  tiietuliules 
enlariic  so  that  their  lumen  is  fre(|uently  double  the  size  of  a 
normal  one  l'"iii.  -<>'.  Ciradually  the  contents  are  moved  to- 
ward the  pelvis  of  the  kidney,  and  finally  are  wasiied  out  with 
the  urine,  or  pressed  and  fus(>d  into  casts. 

To  t'le  latter  we  must  now  pay  ;ittention.  Casts  are  either 
cellular  or  they  are  homogeneous,  p.ile,  transj)arent  hyaline,  or. 
if  thicker  and  more  solid  in  appearance,  waxy:  finally  irranuiar. 
Not  infrequently  they  may  he  mixed  hy  the  adiiesion  ol  cells  to 
a  hy.iline  or  waxy  <iround  matrix  iTijis.  24,  '27.  and  2(Si. 

The  orijiin  of  the  cellular  casts    epithelial,  huikocytic.  hlood- 

ts.  and  the  uraiiular  varieties  can  lie  easily  traced  to  fusion 
of  these  substances  within  one  or  another  part  of  the  tubules. 
Very  difficult  and  disputed,  however,  has  b(>en  the  oriiiin  of  the 
hvaline  aixl   waxy   type: 


(•as 


A  numl)er  of  investiiiators  beli(>ve 
that  tliev  oriLiinate  from  fusion  of  des'|uamated  epithelial  pro- 
toplasmic renmants.  Others,  however,  believe  that  they  are 
the  product  of  an  alltuminous  exudiite  into  the  tubules.  The 
formation  from  fibrin  has  also  ix'cn  advocated,  and  finally  it  is 
held  that  thev  are  the  product  of  a  s])ecific  secretion  of  hyaline 
•ilobules  of  the  epitheliai  cells.  The  literature  on  the  formation 
of  casts  is  very  extensive,  so  that  it  will 
brieflv  review  ;ill  of  it . 


nnpossible  to  even 


Doubtless  you  recall  that  it  was  the  lireat  anatomist  Ileiile'" 
whofiist  discovered  this  rela.tionship.-md  importance  in  comiection 
with  the  iuHammatioiis  of  the  kidney.  Me  interpreted  them  a.s 
fibrin  coauula.     Uovida  ''  later  thorouirhlv  analvzed  them  cliemi- 


DMiKNKUATIVK  AM)  KXIDATIVK  FKATtKKS  OF  NKI'HHITIS    101 


(•ally  and  dcnioiist rated  thorn  as  albuminoid  hodies.  Sin<'e  then 
very  numerous  anatomical  and  exjx'rimental  invest ijiat ions  have 
endeavored  to  demonstrate  their  exact  derivation  and  chemical 
constitution.  Physically  t'.icse  hyaline  casts  are  us"  illy  under 
1  mm.  lonji.  and  the  thickness  is  between  0.01  and  0.05  mm. 
Their  shape  necessaril\'  varies  accordina,  to  the  tubes  they  come 
from;  and  on  their  downward  way  they  are  freijuently  broken  or 
bent.  In  the  kidneys  they  may  be  found  in  all  parts  of  the  tu- 
bules. l)ut  with  particular  frecjuency  in  the  loops,  undoubtedly 
on  account  of  the  mechanical  difficulty  of  propulsion  there. 
\  relat'  )n.shi|)  between  albuminuria  and  cast  formation  does  not 
seem  to  exi.st ;  and  one  may  be  abundant  without  the  other.  This 
fact,  as  well  as  their  aj)parent  different  chemical  constitution,  has 
been  particularly  emphasized  by  those  who  do  not  recoj-iiize  their 
derivation  from  exuded  serum-albumin.  On  the  other  hand. 
\Veiss<ierl)er  and  Perls'"  and  Ribbert  "  are  of  the  opinion  that 
these  casts  rej)re.sent  a  hyaline  transformation  of  exuded  albtnnin. 
It  would  l)e  necessary  to  assume  for  this  a  ferment  action.  Hii)- 
bert  denies  a  derivation  from  desciuamated  and  dejienerated  cells. 
Orth'-'also  recoj-nizes  transudate  casts,  and  in  support  draws 
attention  to  the  occurrence  of  hyaline  masses  between  the  tunica 
propria  and  uninjured  epithelium  in  some  kidneys.  But  he 
further  l)elieves  that  the  previously  mentioned  hyaline  and 
colloid  filobules.  which  ap|)ear  in  the  cells  durin<>;  the  process  of 
parenchymatous  defieneration,  may  be  discharjjed  and  fuse, 
with  the  formation  of  casts.  He  calls  these  "secretion  casts." 
Similar  are  tlie  views  of  Landsteiner.^'  who  hokis  that  hyaline 
bodies  develop  in  the  epithelial  cells  as  a  result  of  patholofjical 
stimuli.     They  are  discharjied  and  fuse  to  casts. 

Hibl)ert,  on  the  other  hand,  claims  that  such  hyaline  bodies 
may  be  observed  in  healthy  kidneys,  and  that  any  relation  to  the 
formation  of  casts  does  not  exist.    Pfister"  observed  the  occur- 


102 


HKKiHT  S    DISKASi: 


ivncc  of  jii-aiuilcs  within  the  (Ic^ctHTatinjr  cells,  which  rospoiidod 
to  the  Hhiiii  stain  of  Wciiiort,  ami  also  in  other  staiiiiii<i  (jiialitics 
rescmhlcd  casts.  Similar  had  Imhmi  the  views  of  Henle,  and  later 
Klel)s.  Israel,  and  Krnst,''  who  re<>arded  them  as  fihrin,  particu- 
larly as  they  answ(>red  to  Weijrert's  fibrin  stain.  This  has  l)een 
contradicted  l)y  Lul)arsch.'"  who  holds  that  other  substances  <!;ive 
similar  reactions,  and  that  the  diajinosis  of  fibrin  must  be  made 
on  morj)holo<iical  as  well  as  tinctorial  jirounds.  Much  confusion 
has  arisen  over  the  nature  and  .sijiiiificance  of  •  vaxy  casts.  They 
have  been  rejiarded  by  some  as  amyloid,  on  account  of  certain 
reactions,  but  they  occur  in  all  forms  of  nephritis,  are  of  variable 
reaction,  and.  in  all  probability,  are  not  amyloid. 

Lyon''  rejiards  casts  as  either  a  coaj-ulation  of  an  intratubular 
transudate  or.  in  the  majority  of  cases,  arisinj:  by  firanular 
disintegration  or  colloid  transformation  of  secretinjr  cells. 

It  api)ears  that  all  casts  are  prol)ably  not  of  definite  uniform 
character  and  derivation.  This  is  made  likely,  not  only  by  the 
nuiltitude  of  ob-servations  of  their  derivation,  but  more  so  by 
their  extremely  variable  morpholofiy  and  chemical  character, 
as  is  particularly  well  shown  in  their  ditTerent  staininj:  affinities. 
Sometimes  they  stain  faintly  with  eosin,  sometimes  rather 
deeply;  occasionally  they  seem  to  have  some  affinity  for  basic 
stains.  With  iodin  they  stain  from  dark  l)rown  throujjh  all 
shades  to  yellow;  with  methyl-violet,  blue,  but  also  violet  or 
pinkish.  On  the  other  hand,  waxy  casts  never  <iive  the  iodin- 
sulphuric-acid  reaction  for  amyloid,  and  are  better  termed  colloid 
casts,  to  avoid  confusion. 

I  therefore  believe  that  the  oriuin  of  these  casts  depends 
upon  several  factors,  and  is  inconstant.  l']j)ithelial  cells,  by 
uranul.'ir  disintejiration  and  ubsequent  hyaline  transformation, 
can  apparently  furnish  material  for  their  formation,  and  this 
process  can   b<>  directly  demonstrated   in  all  stajies.     That   a 


DK(JKNKKATIVK  AND  KXIDATIVK  KKATIKKS  OK  XKl'HKITIS   103 


colloid  secretion  is  fiirinslieil  l)v  the  epitiiplium  is  not  probable, 
but,  more  likely,  that  a  colloid  dejieneration  or  transformation 
of  the  cells  as  Lyon  expresses  it  contributes  toward  them. 
Finally,  it  appears  that  both  of  these  substances  may  fuse  with 
inflammatory  ali)uminous  exudate.  We  can  recojinize,  there- 
fore, these  three  factors  that  enter  into  cast  orifjin,  and  as  one 
or  the  other  predomiintes  or  may  be  absent,  the  character  of 
the  cast  varies  physically  and  chemically.  These  views  are 
further  supported  by  the  observations  of  Litten."^  who  demon- 
strated not  only  the  participation  of  coajiuhited  epithelial 
matter,  but  also  the  addition  of  trajisuded  serum-all )umin;  and 
Lanfjhans,'"  who  saw  not  only  epithelium,  luit  also  chanjted 
leukocytes  and  red  blood-cells  enteriufi  into  their  com])ination. 
That  in  the  presence  of  much  disintesirated  cell  material,  fer- 
ment action  may  play  a  role"'"  to  further  change  the  constitu- 
tion of  these  substances,  and  cause  coajriilation,  seems  likely. 
Hibbert  contends  that  the  acid  reaction  of  the  urint  may  be  a 
factor  in  the  coajjulation  of  albuminous  matter  to  casts. 

A  few  words  about  cvlitidroids.  These,  as  you  know,  are 
pale,  lonji.  tortuous,  narrow,  usually  distinctly  striated  bands  or 
ribbon-like  formations.  One  end  is  usually  rounded,  while  the 
other  extremity  frequently  presents  a  torn,  fibrillated  appearance. 
Some  hold  them  closely  allied  to  hyaline  casts;  others,  however, 
— and  I  .share  the  view, — believe  that  they  are  mucoid  threads, 
which  owe  their  orijiin  either  to  prostatic  secretion  or  secre- 
tions from  Cowix^r's  and  Lit t re's  jilands.  They  occur,  some- 
times in  otherwise  normal  urine,  in  jireat  abundance,  but  particu- 
larly with  other  nuicoid  and  slimy  matter.  On  the  other  hand, 
they  do  not  seem  to  have  any  relation  to  the  inflammations  of  the 
kidney,  and  I  have  never  seen  anything  in  kidney  sections 
which  resembled  them.  This  makes  it  probable  that  they  owe 
their  orijrin  to  other  parts  of  the  fjenito-urinary  tract. 


104 


HI{l(;HT  S    DISKASi: 


Thirdly,  the  cli.iiijrcs  iti  the  iiitcrtuhular  interstitial  tissue. 
This  is  not  only  the  support  in-:  connect  iv('-tissu(>  frame  of  the 
parenchyma,  but  tin-  carrier  of  liloctd-vessels.  lymphatics,  and  the 
nerves,  '{'he  chanires  occurrinj:  in  it  are  partly  <le|«'ndent  on  a 
primary  involvement  (»f  these  structures,  hut  l;irji:el.v  also  upon 
the  modifyinii  influence  which  the  involvement  of  one  of  these 
parts  exerts  upon  the  other.  On  the  other  hand,  it  is  influenced 
in  turn  hy  th(  patholo-iical  relations  of  the  nei«ihl)orin<;  parenchy- 
matous structures.  To  make  this  cle.ar:  The  chanjies  in  the 
l»lood-ves.><els  hritiu  about,  of  necessity,  alterations  in  the  lym- 
|)liatics,  which  auain  reflect  upon  the  va.sciilar  apparatus 
and  the  surroundinj:  comiective  ti.ssu(>.  But,  further,  while 
the.se  chaiiiies.-dTect  the  tuhules,  their  disturbances,  by  nece.ssary 
interchanire,  cau.se  subsecjuent  patholo<;ic;d  alterations  in  the  in- 
terstitial tissue.  It  will  liive  you  ••m  idea  how  intimately  all  these 
various  structures  are  related,  and  that  much  of  the  c(miplex 
picture  of  the  disease  is  not  nece.ssarily  the  result  of  direct  injury 
or  in v.ision,  but  a  .subseipient  development ,  the  result  of  disturbed 
anatomical  relations.  This  accoimts,  in  no  small  de<:ree,  for  the 
jireat  individual  variations  which  we  daily  meet  in  all  diseases. 

The  flrst  chan<i<'  which  this  interstitial  tissue  shows  is  inflam- 
njatory  hypenemia.  This  leads  to  compression  of  the  rest  of 
the  interstitial  substance,  lymphatics,  and  tubules.  Resorption 
must,  therefore,  be  interfered  with  from  the  Iw^nnniiifr.  Clo.selv 
f()Ii.)witi;i  is  the  development  of  inflannnatori-  (edema.  This 
nuist  lie  .ittributed  to  slowinj;;  of  the  blood-current,  increased 
permeability  of  the  v(>s.sel-walls,  and  lack  of  resorption  on  the 
part  of  the  lymphatics.  This  inflanmiatory  irdema  leads  to 
imbibition  of  the  coimective-t issue  structures  and,  as  we  .saw  be- 
fore, the  epithelium  of  the  surroundinji  tubules.  The  comieetive- 
ti.ssue  fibers  .separate,  become  stretched,  jrla.ssy,  pale,  inflexible; 
and  stafjnation  of  blocxl-and  lymph-streams  follo\  ^.   Then  occurs, 


i)k<;k.\ki{.vtivk  and  k.mdativk  kkatikes  ok  nki'iihitis  Kt") 


I"i(f.  •_'!».     r(ii(jl<iin(iiil;ir    iiitcrstiliiil  cell  iiitillratioii  iiroiiii<l  .-i    hyaline  nloincnilns.     Tlir 
adjoinitiK  tiiliiilcs  rimcli  dilated.      X  240. 


DKdKNKUATIVK  AM)  KXl DATIVK  KKATl  HKS  OK  NKPHUITIS    107 


first  patchy,  hut  IwcominK  streaky  and  finally  diffuso,  a  collular 
exudation,  around  ^clonieruli  and  l)otw(M«n  tubules  ( Fijr.  29).  The 
emigrated  cells  lod^e  in  lymphatics  and  tissue  spaces,  producing 
a  lyniphanjiitis  and  ix'nlyniphanjritis.  They  projrress  within 
these  preformed  channels,  but  also  jjet  into  the  tubules,  particu- 
larly attracted  by  necrotic  and  de>ieneratin<i  portions.  The 
character  of  these  cells  varies  in  different  tyjK's  of  inflammations 
and  different  stages  of  the  process.  (*ouncilinan  has  shown  that, 
particularly  in  certain  of  the  acute  exanthemata,  the  whole 
exudate  may  consist  primarily  of  so-called  mononuclear  i)lasma 
cells  and  emijrratinfj;  lymphocytes.  Later  in  the  process,  as  the 
parenchymatous  destruction  becomes  manifest,  |K)lymorphonu- 
clear  types  prevail. 

The  exudate  contains  most  always  some  red  blood-cells,  and 
sometimes  streaky  or  diffuse  hemorrhajies  occur.  This  is 
noticeable  particularly  in  scarlet  fever  and  in  other  severe  septic 
infections  which  have  a  tendency  to  marked  injur>-  of  the  vessel- 
walls.  The  blood  is  discharjjed  into  the  tissue  spaces  and  tubules. 
In  these  more  severe  cases  fibrin  is  also  present.  Under  these 
circumstances  the  kidney  l)ecomes  succulejit.  softer,  and  an 
abundant  turbid  fluid  may  l)e  squeezed  out  on  section. 

However,  these  are  not  the  only  chaufres  wiiich  are  promi- 
nent in  the  interstitial  tissue.  Connective-tissue  and  endothelial 
cells  underjio  cloudy  swelling'  and  fatty  chanjies.  The  latter  may 
become  vory  marked,  and  lead  toaccun)ulation  of  abundant  fat- 
drops  in  the  interstitial  tissue  and  within  tissue  and  lymphatic 
spaces.  Lohlein"'-  repirds  this  as  an  indication  of  resorption. 
The  fatty  sul)stances  are  partly  ordinaiy  fat,  partly  doubly 
refractin<c  myelin  substances,  and  partly  a  cr>-stalline  protafjon- 
like  l)ody.  I  will  discuss  these  matters  in  detail  in  connection 
with  fatty  degenerative  nephritis.  It  remains  to  sketch  the 
functional  disturbances  thus  induced. 


t 


I  OS 


HUKiMT  S    DISKASi; 


Tlic  scvric  tliimjics  in  the  ^tlomcnili  nrul  tuNiiU's  ncci'ssarily 
lend  In  ;i  innrkcd  diniiiiutioii  in  the  iiiiiouiit  of  urine,  .soinetinies 
to  alinosl  Mil  ;iiiiui;i.  'riic  urine  llius  U'conies  ne<'essarily  liiyli 
colored.  :ind  fimdu.illy.  as  e\u<l:ite  and  cellular  detritus  a|)|)ear  in 
it.  turhid.  and.  as  hlood  a|)|)ears.  smoky.  'I'he  specific  jxravity 
is  hi;ili.  and  this  in  spite  of  the  fact  that  the  normal  urine  constit- 
uents are  markedly  diminislu'd.  This  is  not  only  due  to  the 
v;reat  concentration  of  the  urine,  hut  tmu'e  especially  to  the 
pres<'nce  of  l;irv,('  :imouiits  of  seruni-alhumin.  with  nucleo- 
alliumiii.  the  former  Ix-iiif:  tlerived  from  the  ahundant  exudate 
and  free  Itlood.  the  latter  from  the  cellul.ir  destruction.  Mor- 
pholouically,  such  a  urine  contains  all  varieti(s  of  cells  of  the 
exudate:  leukocytes,  free  Itlood-cells,  mononuclear  cells,  and 
a  lary:e  numl>er  of  desijuaniated  and  iiewiy  formed  epithelial 
cells.  Necrotic  cell  mass(>s  are  also  present.  Ca.sts  are  very 
numerous  hlood.  leukocytic,  epithelial.  f>raiiular.  fatty,  hya- 
line, and  waxy,  with  the  cellular  type  predominatiii"!.  .Many 
of  the  hlood-cells  underii(»  Iwemolysis.  .settinjr  tli(>  pijimeiit  free, 
which  adds  to  the  characteristic  smoky  color  of  the  urine. 

These  evidences  vary  necessarily  with  the  predominance^  or 
ahsence  of  tlie.se  patiiolo;.ncal  chaiifies.  and  this  leads  me  to  say 
a  few  words  ahout  these  variations  and  their  prohahle  cause. 

\()  douht  you  appreciate  that  what  I  have  presented  to  you 
here  is  a  composite  picture,  suhject  to  many  individual  modifica- 
tions. Out  of  the.se  we  can  recoiMiize  two  larger  jrroups:  one 
in  which  the  proce.ss  is  related  more  particularly  and  ener«>:etically 
to  the  vascular  apparatus,  and  one  in  which  the  process  is  pre- 
d()minatin;rly  dejrenerative  and  proliferative  amonji  the  fixed 
cells  of  the  kidney.  .\s  one  or  the  other  pnvlominates  and  in- 
fluences the  later  manifestations  of  the  disease,  we  c;in  recofjiiize 
that  exudative  or  dejienerative  and  proliferative  features  pre- 
dominate, and  therefore  jrive  t(;  the  whole  lesion  a  characteristic 


DMiKXKHATIVK  AM)  KXIDATIVK  KKATfUKS  OK  NKPHKITIS    109 


stump.  The  caiisf  for  this  lies  iiii(loul>t('(lly  not  only  in  the 
(|iU'stion  of  <|U;inlitativ('  irritation,  hut  in  the  iwculiar  affinity 
which  cc'rtaiii  invasions  have  for  «»n('  or  tlu'  otlx-r  tissue.  It  has 
iwi'ii  found  hy  Mauni<;art(>n.  for  instance,  that  the  intro(lu<'tion  of 
tulxTcle  liacilli  leads  ni.iinly  to  the  fo'ination  of  <rranulon)atous 
ti.s.sue.  while  the  introduction  of  the  toxin  without  i)acteria  is 
followed  iniiinly  i>y  exudative  processes.  The  .s;inie  fact  .applies 
to  other  intoxications  and  poisons.  Snake  venoms,  f(»r  instance, 
have  a  fireater  destructive  and.  therefore,  reactive  effect 
on  the  vascular  apparatus.  In  .scarlet  fever  this  has  Ion;;  In'en 
reco^inized.  On  the  other  hand,  certain  dis<*ases  and  |M)i.sons 
exert  the  greatest  destructive  inffuence  on  the  fixed  cells,  and 
their  lesions,  and  results  therefrom,  .-ire  more  evident  and 
dominating  in  such  cases. 

Certainly  it  would  lie  a  mistake  to  endeavor  to  draw  lines  of 
mathematical  distinction  l)Otween  these  various  manifestations. 
In  the  end,  we  are  dealing  with  one  or  another  accentuation  of 
fctitiirt's  of  a  nephritis,  not  with  independent  distinct  disea.ses. 
It  is  only  for  th<' jnirpose  of  study  that  we  can  divorce,  or  abstract 
them  from  the  others,  thus  lifting  them  above  concomitant, 
correlated,  and  dependent  changes. 


lOriMH   LKCTlHi:* 

I'm;  IJksi  i.Ts  wd 'I'kumin atiun^  (ik  l)i;iiK\Kii  \ti\  k  and  \'.\\- 
datim;   NKi'iimris,     I'iiudi  iti\  k    ('iiwiiKs    i\    thk 

KlIlNKV 

(it  n III  nil  II : 

We  liMVf  followed  the  iicpliritic  process  to  the  lieijilit  of  its 
(U'veiopinetit.  \Vli;it  .•lie  its  teniiiiiiitiolis?  'I'liey  ;iie  tliree: 
first,  f.'ital;  secoixi,  MtteDiiatioii,  with  eertaiii  tiXMliticatioiis  in 
theinfi.'iiiiiiiatioii.  which  allows  progress  in  a  less  l)rus(|iie  iiiaiuier, 
ami  therefore  extends  over  a  prolon^^ed  jM'riod  of  time;  tliird, 
latency,  with  (onstant  daiijrerof  exacerbation,  and  ultimate  fatal 
tenninati')!!.  I  have  not  included  recctvery  in  this  list,  liec;iuse  I 
consider  it  extremely  doul>tful  wlx'ther  actual  restitwtictii  to 
intejirity  ever  occurs  in  severe  nephritis,  and  wh<'ther  it  can  (>ver 
he  rejiarded  as  healed  or  cured,  in  the  sense  in  which  these  terms 
are  ordinarily  employed.  If  you  recall  for  a  moiiicnt  • .  <>  seveu 
destructive  chancres  which  we  observed  in  the  glomeruli,  and 
the  anaton)ical  arranj;ement  of  the  <ilomerulus,  you  will  probably 
ajrree  that  the  structure  has  not  only  iH'en  jH-rinanently  injured 
and  destroyed,  but  that  rejteneration  to  it:^^'  former  state  must  l)0 
out  of  (juestion.  It  is  true  that  alls  may  rejicnerate  rapidly, 
but  this  retjuires  that  the  anatomical  arranjicment  of  the  part 
has  not  been  lost ;  it  remains  confined  to  <'ells  within  established 
structures.  The  tuft  once  destroyed  in  a  jilomenilus  c.innot 
reproduce  a  new  one.  Xo  one  has  ever  seen  new  jilomeruli  or 
tubules  form,  nor  even  a  new  tuft  within  an  old  jjlomerulus 
capsule.'  This  destruction  remains  a  permanent  loss,  and  the 
orpmism  must  help  itself  in  some  other  way.     Undoubtedly, 

•  Drlivirr;!  1.11  K.'hriiarv  !!,  VMM. 
Ill) 


tJKtiKNKMATIVK    AM)   KXl'DATIVK    NKI'llurTIS 


111 


many  jjlonirnili  have  not  Im'cii  injun-d  to  such  cxtrnt  a.s  to  call."**' 
ciitin'oltjitrration  of  thr  tnft.  .\nii>lioratioi)  of  tin*  inflanunation 
will  niak<'  |M»s.sil»l<'  at  Irast  soinr  functional  activity  in  houh'  mon- 
than  in  otlu'ix;  howevrr,  the  |)atholo};ical  chanj^cs  in  thcni  hav«' 
at  least  jXTniancntly  affected  the  normal  structures,  and,  while 
not  com|)letely  ainiihiiatin^  them,  leave  them  in  an  injure<l 
state,  constantly  in  danjier  of  inflammatory  exacerh.itions. 
'Phis  is  particularly  unfortun.-iteand  dangerous,  inasnuich  as  they 
;ire  called  u{)on  to  increase  their  work  in  order  to  com|HMisate 
those  which  have  Imh'Ii  entirely  elitninated.  This  necessary- 
increased  functional  activity  and  irritation  make  them  mon> 
vulneral)le  and  hasten  the  ultimate  fate  of  final  destruction.  In 
the  tuhules,  as  we  will  learn  pres<'ntly,  a  very  simihtr  state  of 
affairs  exists.  Indeed,  strong  evidence  has  gradually  accunuilated 
which  points  to  tlie  fact  that  many  of  the  .s()-calle<l  primarj' 
contracted  kidneys,  or,  l)etter.  cases  of  productive  nephriti.s, 
are  really  of  the  so-called  secondarj-  ty|K»;  that  they  found  their 
orifiinal  .start  in  a  dejienerative  exudative  nephritis,  .sometimes 
fifteen,  twenty-four,  or  twenty-eijiht  years  ajro,  most  frequently 
during;  the  course  of  a  .scarlet  fever.  The  recover}'  in  the.se  cases 
wasonlyapparent ;  the disea.se  continued  slowly  hut  projtre.ssively, 
in  a  manner  to  which  the  orjjanism  adapted  it.self,  and  therefore 
enjoyed  relative  health  for  years,  until  the  disease  had  finally 
reached  a  stajte  when,  as  out  of  a  clear  sky,  a  fatal  catastrophe 
occurred.  In  reality,  therefore,  of  very  lonj;  duration.  Clinicians 
like  Heuhner  and  Dixon  Mann  have  long  empha.sized  such  cases. 
Only  recently  F.  .Miiller-  said:  "'The  kidney  is  a  treacherous 
orjran.  which  may  carrv'  latent  an  injur}'  for  decades,  to  finally 
cause  sufferinji  and  death." 

.Most  convincing  are  the  observations  of  Ixihlein,'  ljecaust> 
they  furnish  an  objective  anatomical  basis  for  these  ideas.  I 
hjive  already  touched  ufK)n  them  in  the  first  lecture,  but  yoi    vll 


112 


nUKillT  S    DISKASK 


n'c;ill  tliMt  he  found  lliat  tlicsc  s()-c;illc(l  s('c()iul;irv  (•oiitnictcd 
kuliu'vs  arc  iniicli  more  frcMjiiciit  lliaii  supposed,  and  iiiav  he 
fracod  to  previous  stages  of  dejiciierative  and  exudative  uephfitis. 
lie  also. you  recall,  drew  attention  to  a  type  of  cases  which,  haviuji' 
pa.ssed  thfouirli  a  so-called  acute  attack,  enjoyed  felative  iiealth. 
.iTid  then  suddenly  died  witii  all  the  syiriptoms  of  nephritis.  In 
them  he  found  typical  pfoductive  jiloincfulonephritis  with 
marked  contraction  of  theoriran:  the  process  nuist  have  jrone 
on  insidiously,  hut  no  less  perniciously,  for  years.  Similar  are 
the  views  of  .\ufreclit. 

My  own  observations  in  the  matter  fully  corrohorate  the.se 
contentions,  and  I  am  of  the  opinion  that  at  least  the  majoritv 
of  (•.•i.ses  of  late  nephritis  have  been  ushered  in  hy  previous 
deirenerative  exudative  lesions,  which,  havinii  become  latent, 
have  been  disre;iarded  clinically  until  their  proufess  has  led  to  a 
point  where  the  orfranisin  is  unable  to  adapt  it.self.  Then  it  pro- 
duces manifestations  which  ap|)ear  n(>w  .and  stidden.  but  mijiht 
h.ave  been  .anticipated  lonu'  ai^o.  riKpiestionably.  this  has  much 
pnictii-al  be.arini;  in  the  matter  of  pro;rii<»sis  and  in  the  matter  of 
treatment  also.  ( >ne  should  l)e  very  cautious  in  niviiii:  an  opti- 
mistic ultimate  projrnosis  in  any  deucnerativeexud.ative  nephritis, 
.and  no  doubt  many  mon'  cases  of  nephritis  i-ould  be  benefited  bv 
treatment  if  they  were  more  carefully  watched  for.a  lon^  tim(>  after 
the  evidences  of  the  i>ru.s(iue  initial  lesions  had  subsided,  and 
later  at  intervals.  Mut  here,  as  in  other  diseases,  a<lvice  is  not 
souirht.  and  the  early  staiics.  still  amenable  to  treatment,  are  dis- 
rciiarded  by  the  p.iticnt.  and  unfortunately  also  by  the  phvsician. 
Both  usu.ally  pay  no  attention  lo  a  dise.a.se  until  it  becomes 
m.anifest  in  .an  entire  upset  of  ;in  oriianism's  economy.  Phv- 
sicians  are  not  alw.ays  at  f.ault  .at  this.  ( )ur  diagnostic  methods 
at  the  best  are  indelicate,  and  irive  inform.ation  only  in  .severe 
interferences.     Mut  it  .seems  that  nnich  of  the  coi  d  careful 


DF:(iKNKIfATI\  K    AM)    KXIDATIVK    NEI'UKITIS 


ll.i 


()l)S('rvati()n  h;is  pjissod  out  of  medicino  in  a  hasty  jjrojiress. 
Perhaps  the  old  physician,  in  spite  of  his  hick  of  knowledge,  may 
have  been  unconsciously  a  l)ottor  physician  in  many  instances. 
His  close.  const-Hit,  and  friendly  a.ssociation  with  patients,  whom 
he  frecjuently  .s  w  and  consuit'd  with,  allowed  him  i)erhaps  to 
form  much  ear,  i  nd  hetter  opinions  of  ex{)re.ssion  of  disea.se 
than  we  are  now  al>le  to  alt.iin  with  our  hasty,  purely  objective 
methods.  .Much  u.sed  to  enter  into  the  lejiitiniate  practice  of 
medicine  which  now  has  passed  away  for  lack  of  time,  or  has 
been  consumed  by  the  charlatanism  of  schools,  and  exafijrerated 
l)y  uneducated,  unrefined  followers.  Dilettantism  and  notoriety 
to-day  march  under  the  flaji  of  l)road  scientific  knowledjie  and 
busine.ss  methods.  I\H)ple  for<ret  that  the  human  mind  can  only 
do  relatively  few  thiiif^s  thorouj-hly  and  reliably,  and.  therefore, 
that  in  science  and  art.  imlike  Inisiness.  quantity  never  <j;oes 
with  (jualitN .  .Nowhere  are  careful,  painstakinjr.  and  hmji- 
continued  observation  and  treatment  more  stronjrly  indicated 
and  of  fireater  importance  to  the  patient  than  in  nephritis. 

We  shall  now  proceed  to  consider  in  detail  the  further  chan<ies 
in  the  kidney.  conmiencin<r  with  the  time  we  reached  at  the 
end  of  the  la.st  lecture. 

.\fter  the  proces.ses  of  parenchymatous  destruction  and  exu- 
dation have  attained  the  heijjht  to  which  we  traced  them,  there 
occurs,  provided  that  the  individual  does  not  die,  a  relative 
standstill.  By  this  do  not  misunderstand  that  thinjrs  halt 
entirely,  but  the  process  has  arrived  at  a  point  where  rapid 
pro;;re.ss  and  uniformity  of  dejienerative  and  exudative  phenom- 
ena stop  and  evidences  of  rejrre.ssion  and  attenuation  become 
visible,  jiradually  leadinji  to  new  patholojiical  proce.s.ses,  which 
liive  to  the  whole  a  <rn>ater  variety  of  pictures.  This  depends 
probably  upon  complex  (jualitative  as  well  as  (juantitative 
chanfies  within  the  kidnev  and  the  irritant.     It  wouhl  lead  me 


I 


^1 

If 

•■(: 


114 


UliKillT  S    DISKASK 


here  too  far  to  enter  into  a  detailed  discussion  of  tliis  (luestioii, 
hut  I  will  oiilv  indicate  to  vou  that  this  nuist  i)e  attril)Uted.  first. 


to   tlie  chaimes   which   the   iiiflaimiiati( 


)ii 


as  proc 


luced 


HI     tl)( 


th 


tissues  of  the  kidney  and  in  their  anatomical  airanfreinent .    Into 
this  natuially  enter  the  (|ualitative  clian,ii(>s  within  the  cells  and 


niech; 


inical  factors  due  to  the  reai  ranirenien 


tofti 


le  parts.  Secoiu 


owini;;  to  the  chaniics  in  the  irritant  hrou^ht  ahout  i)y  the  in- 
flammatory condition  of  the  orjran.  much  of  it  has  been  directly 
destroyed,  or  .-it  least  altered.  Moth  thes(>  points  are  complex  and 
intricate,  and  involve  many  other  problems,  and  I  therefore  can- 
not fully  discuss  them  within  the  scop(>  of  these  lectures.  Suffice 
it,  therefore,  if  you  api)reciate  that  tiie  inflanunatory  alterations 
in  the  structure  of  the  kidney  and  the  concomitant  chanii'ed  rela- 
tionshipto  the  inflammatory  irritant  havedrifted  toa  jjoint  where 
the  oriiiinal  response  of  the  tissues  to  the  invasion  iiecessarilv 


ceases  .and   undermu-s  < 


<leci(led  modifications.     These  modific; 


tions  in  the  inflanmi;itory  process  are  expres.sed  in  two  main 
changes:  first,  lessened  exudai'  iii;  and,  .second,  fatty  deiienera- 
tion  and  infiltration  of  the  remainiiii!-  i)arts.  They  result  from 
oMitenition  .and  Mockini;'  of  the  iiorm.al  p.aths  of  nutrition  and 
re.<ori)tioii.  ( 'on.se(|uently  mitritive  disturbances  now  connnence 
to  control  the  picture,  associated  iiy  dejirees  with  inflanunatory 
exacerbations  and  remissions,  and.  as  the  subst.ance  wastes, 
more  or  less  extensive  product ixc  ch;in;i('s. 

We  shall  deal  with  the.se  chanucs  in  the  order  here  emmier- 
ated.  I'irst,  then,  the  mitritive  disturbances.  These  m.-mifest 
themselves  in  v.arious  de^ener.ative  processes,  which  either  were 
oriirinally  absent  or  le.ss  i)roi;iineiit.  Colloid  and  hyaline  bodies 
appear  in  ureat  number  within  the  disinteiiratinji  parenchyma 
cells;  ;iutolytic  processes,  undoubtedly  due  to  ferment  formation 
from  broken-down  cells,  become  coHs|)icuous;  but  the  fattv 
chanucs  ;ire  .apt   to  supersede  all  others  in  prominence.     They 


DK(;EXKUATI\  K    and    KXIOATIVK    XKI'HKITIS 


115 


soon  <ri  <■  to  tho  wiiolo  type  of  nophritis  a  characteristic  appear- 
ance. As  the  result  of  these  various  degenerations,  all  of  which 
iio  alonj:  with  swellin<i  of  cells,  the  kidney  as  a  whole  enlarjres. 
'I'liis  is  further  (hie  to  the  difheulties  in  resor[)tion  and  nutrition 
of  the  parts,  to  capillary  a!id  lymphatic  obliteration,  which 
allows  hroken-down  material  to  collect  and  stajrnate.  It  is  also 
added  to  by  the  presence  of  inflammatory  cedema,  and  the 
occasional  exudative  exaceri)ations.  All  of  these  contribute  to 
a  uradual  but  very  marked  increase  in  the  size  of  the  orjian  and 
an  obliteration  of  its  nortnal  m.arkinjrs.  Thf^se  jrive  way  to  a 
more  uniform,  aiia-mic,  yellowish-pale  color,  interchan<tinfr  with 
areas  of  vascular  injection  where  the  process  is  exudative  or 
productive,  or  where,  due  to  obliteration  of  old  normal  channels, 
compensatory  dilatation  of  vascular  canals  has  occurred.  At  this 
point  of  the  process  the  capsule  still  strips  (>asily,  the  surface 
bulfics  very  prominently,  as  .so,  on  section,  does  the  cortex.  The 
normal  markinirs  appear  lost  or  nnich  distorted.  The  jilomeruli 
;ire  pale  !iiid  <:lisieniim-.  the  medulla  dull  pale  yellow  in  color, 
and  the  line  of  demarcation  between  it  and  the  cortex  poorly 
accentuate<l.  In.  short,  it  pre,«<ents  the  kidney  now  spoken  of  as 
chronic  paienchymafous  nephritis,  or  larjie  white  kidney;  better 
aiul  more  correctly,  as  I  t(>rmed  it  at  the  bejiinninii  of  the.se 
lectures,  the  de.!i(>nerative  fatty  nephritis.  Inasnmch  as  these 
fatty  sub.-;tances  play  such  a  role,  we  nnist  have  a  clear  picture  in 
our  mind  what  they  are.  and  what  is  their  derivation  and 
siunificanc(  Here  we  enter  another  very  nuich  di.sputed  and 
much  foujihl  over  liround  of  jieneral  patholofiy.  Vou  nuist, 
therefore,  be  content  with  a  .short  .summary  of  the  situation. 

Vou  are  aware  that  X'irchow  '  orijrinally  distinjiui.shed  between 
two  ty|>es  of  fatty  chanjies:  de<i;eneration  and  infiltration.  In 
the  latter  he  assumed  that  the  fat  was  broujiht  to  the  part,  while 
in  the  former  occurred  a  direct  transformation  of  the  protein 


no 


UKKiMT  S    DISKASK 


portion  of  the  protoplasm  into  fat.  This  involved,  tl  an 
acti»('  and  niucli  more  severe  permanent  destruction  of  the  pro- 
tophism.  while  infiltration  was  passive.  Support  of  this  idea 
eame  in  the  celebrated  ohservatiotis  of  von  Voit  and  Petten- 
kofer, '  later  followed  by  others,  particularly  Hauer  and  V.  Hof- 
inan.  and  followed  by  the  critical  review  of  Pflii^er.''  The  latter 
demonstrated  tliat.  althouirh  a  direct  transformation  of  protein 
into  fat  cannot  be  denied,  there  is  no  sufiicient  proof  that  this 
actually  occurs.  If  at  all  possible,  it  seems  most  probable  by  a 
primary  splitting;  otT  of  carl)on-poor  decompo.sition  products, 
with  a  following  synthesis. 

For  these  rea.sons.  and  particularly  on  account  of  jiradually 
accumulatiufi  experimental  evidence,  the  idea  of  fatty  dejienera- 
tion  became  "gradually  replaced  by  that  of  fatty  infiltration.  It 
is  particularly  to  liosenfeld"  that  we  owe  the  most  convincin<t 
testimony  in  its  favor.  He  determined  the  ether  extract  of 
normal  orjians  and  compared  it  with  that  of  fatty  ones.  He  and 
Humpf  "^  ob.served  a  variable  but  decided  increase  from  25  per 
cent,  to  '.H),  4(t.  (>().  and.  in  phosphorus-poisoninji.  even  75  j)er 
cent.  These  l.irjie  percentafies  ap{)eare(l  to  Hosenfeld  as  only 
ascril)able  to  infiltration,  and  he  found  the  proof  in  the  followinji 
in;:('nious  exjH'riments:  If  an  animal  is  made  practically  fat-free 
by  starvation,  and  then  fed  with  a  forei<rn,  easily  recojinizuble 
fat.  as  nuitton  fat.  cacao-butter,  line  oil.  this  may  easily  be 
detected  in  the  normal  fat  depots  of  the  body.  Now.  if  such  an 
animal  is  poisoned  with  phosphorus,  or  some  other  sul)stance 
leadinj:  to  marked  fatty  dejreneration,  the  fatty  dejienerated 
orjjans  are  foimd  to  contain  this  foreign  fat.  If,  on  the  other 
hand,  such  animals  were  simply  starved  and  then  poisoned,  fatty 
de^ieneration  did  not  occur.  I.A'lH'detT''  has  nuule  similar  obser- 
vations in  starved  human  beinjis,  with  the  same  result.  The 
previous  i n vest i<iat  ions  of  Lusk'"  and  his  pupils  on  phosphorus- 


DK(iENKUATIVK    AND    KXIDATIVK    NKPHRITIS 


117 


|)<)is()ninK  liad  iilroady  domonst rated  the  infiltrative  character 
of  these  fatty  changes,  and  he  interpreted  them  as  an  attempt  on 
the  part  of  injured  cells  to  keep  themselves  alive.  He  therefore 
sjK^aks  of  suKar-hvmfiry  cells. 

An  interestiiifi  observation  was  also  made  hy  Fischler,"  who 
carried  soap  solution  throufjh  excised  kidn'~vs,  and  ol)taine(l  in 
this  way  the  picture  of  fat  dejieneration.  tie  accomplished  the 
same  by  usinjr  l)lood,  .soap,  and  «ily<'fnn.  From  this  it  was  c(m- 
cludcd  that  the  fat  is  brought  to  the  parts  in  soluble  form. 

Rosenfeld  found,  further,  that  there  exists  a  distinct  relation 
l)etween  the  jilycofjen  content  and  fat  de<:eneration.  The  latter 
docs  not  occur  in  the  presence  of  the  former,  and  if  jrlycofien  is 
administered  to  animals  poisoned  with  phloridzin,  the  fat  de- 
•ieneration  diminishes.  He  interprets  this  similar  to  Lusk: 
Fat  and  fiiycojien  fvirnish  fuel  for  the  purpose  of  defen.^e  ajiainst 
toxins,  and  compensate,  therefore,  a  lost  protoplasmic  portion 
of  the  cell.  Ro.senfeld,  therefore,  speaks  of  fat  rej^eneration,  in- 
stead of  fat  dejieneration. 

Xow,  patholofrists  have  alwjiys  hesitated  to  accept  the  idea  of 
pure  fat  infiltrati(m  for  all  fatty  chanjies  in  or<cans.  and  mainly 
on  morpholojiical  considerations.  You  know  well  that  the  ap- 
jK'arance  of  fat  in  cells  fioes  alon^  in  certain  cases,  just  as  Vir- 
chow  ol)serve(l  it,  with  protoplasmic  de.struction,  and  ajiain  with 
relatively  jiood  preservation  of  the  cell  constituents.  For  the 
first,  pathological  anatomists  have  retained  the  term  of  fatty 
(lejieneration,  and  for  the  second,  fatty  infiltration.  Very  soon 
evidence  ac<'unuilated  which  again  brought  new  .support  to  these 
old  but  |)erfectly  justifiable  conceptions.  In  the  first  place,  it 
was  found  that  the  apparently  very  clear  conclusive  observations 
of  Ro.senfeld  and  others  hail  notable  exceptions,  inasmuch  as  in 
.some  fatty  degeneratetl  organs  -the  kidneys,  particularly— the 
fat  content  was  not  only  not  always  increased,  but  occasionally 


I 


lis 


UliKillT  S    DISKASi: 


Mctiuilly  <liiiiiiiisli('(ll  How  cmm  this  \)v  cxpliiiiicd?  Ilxplaim- 
tioii  of  this  |»h«'iioiii('noii  ciiiic  from  another  source. 

If  oriiaiis  are  i<e|)t  niider  entirely  aseptic  con(iiti(»ns,  there 
Mccins.  as  you  kiKtw,  a  |>ost -mortem  softeninj;.  This  is  especially 
well  illustrated  in  certain  inflamed  oriians,  [)articularly  the  lunjis, 
whii'h  are  ri<'h  in  exudate.  This  s(»ftenin!H',  or  autolysis.'-'  is 
accompanied  liy  the  ap|)earance  in  the  cells  and  tissues  of  an 
abundance  of  iiranules.  somewhat  similar  in  mori)holo^ical  aj)- 
pearance  to  the  chauiics  we  ol».ser\-e  in  the  process  still  called  fat 
deucneration  and  in  late  parenchymatous  (lejicneration.  These 
small  fat-appeariuu  <lroplets  ditVer,  however,  in  certain  impor- 
tant jiliysical  and  chemical  respects  (juite  markedly  from  the 
ordinary  neutral  fat.  i.<..  the  combination  of  jilycerin  with  a 
fatty  acid  radicle.  Physically,  these  substances  are  charac- 
terized by  double  refraction  of  polari/ed  liiiht  ;  chemically,  by 
a  marked  dirt'erence  in  constitution  from  ordinary  fat,  and  de- 
composition with  fre(|uent  formation  of  jrlyeerin  phosphoric  acid. 
While  such  bodies  have  been  known  for  a  loii^  time  and  l)een 
called  collectively  "myelins"  by  Virchow,  they  a.ssumed  now  a 
new  lijtht  and  importance,  and  have  recently  been  the  field  of 
nmcli  active  investiji.  tioii."  Tiiey  include  substances,  the  most 
familiar  of  which  are  lecithin,  protajion.  cholesterin.  They  have 
also  become  known  under  the  name  of  lipoids,  a  term  introduced 
by  Kletzinski  fifty  years  a^o.  and  reintroduced  by  Overton. 
Connnon  to  all  of  them  is  .solubility  in  ether,  alcohol,  chloroform, 
benzol.  I  caimot  enter  here,  of  course,  into  a  detailed  di.scussion 
of  these  bodies,  but  I  will  illustrate  their  fieiwiil  chemieal  rela- 
tions. 

Our  knowled;>e  of  the  chemistry  of  the.sp  substances  is  still 
very  uncertain,  which  is  larjicly  due  to  the  fact  that  it  has  l)een 
extremely  difficult  to  i.sohite  them  in  the  pure  state.  The  entity 
and  constitution  of  .some  of  them,  at  least,  are,  therefore,  .still 
doubtful  and  uncertain. 


DKCiKNKHATIVK    AM)    KXfDATIVK    NKI'UKITIS 


1!) 


Acconliiiu  to  the  invcstifiMtions  of  Tliiulichum  and  Haii^r.  wo 
may  classify  tliciii  first :  As  pliosphatidcs,  /.  < ..  lipoids  containiiifi 
iiiti()y;(>M  and  |»li(»splionis.  'I'o  this  jiroup  holonji  the  lecithins 
and  the  related  bodies,  kephalin  in  the  brain,  myelin  and  para- 


mvelm  an( 


1  spl 


lyiijromyehn,  o( 
'11 


currinji  also  in  the  brain,  in  e^^ 

ri) 


yellow,  in  red  blood-cells,  and  m  the  snprarenals.  Ihese  repre- 
sent niono-ami(lo-mon()-i)hosi)hatides.  mono-amido-diphospha- 
tides,  (li-amido-mono-phosi)hatides,  and  tri-amido-j)hosphatide, 
the  latter  a  substance  occnrrinji  in  the  kidney. 

Their  chemical  constitution  is  perhaps  best  illu.strated  in  the 


lecithins 


In  order  to  trace  this  structmc  we  have  to  synthetize 


the  decomposition  products. 

(  oinmencinji  with  amm(»nia.  with  which  you  are  all  familiar, 


H 
N    H 


Ainmimiiim 


and  its  livdroxiil 


H 
N    H 


HO 

Aiiimoiiiiim  livilroxid 


we  may  obtain  by  simple  substitution  a  compound  known 
chemically  as  trimethyl-oxy-ethyl  anmionium.  or  more  fre- 
(juently  as  cholin.  an  anunonium  l)ase.  as  follows: 

,('H.-C'H,(OH) 

N  -(('H:0;. 

OH 
Tills  ba.se  may  combine  with  jilycerin  phosphoric  acid: 

("H,(()H) 

('H,(OH) 

CH — O    \ 

OH    PO, 
OH 

in'which  two  of  the  hydrofjens  have  been  replaced  by  two  fatty 
acid  radicles,  say  of  the  stearj-l  f>;roup : 


12() 


HUItiHT  s    DISK ASi; 
•H..     (>     (',JI,,() 

CU.     O    N 

IK)     I'O 

(    HH    () 

N    (CH,). 
OH 


Jiiid  wo  thou  ()l)t;iiii  the  (listcarvl-Iccitliin.  It  will  Ix-  plain  from 
this  foniiula  and  dovclopniont  that  there  is  nioro  than  ono 
kind  of  lecithin,  dependinj;  upon  the  kind  of  fatty  acid  radicle  in 
the  -ilycenii-phosphoric-acid  j-roup  of  the  compound.  We. 
therefore,  have  also  palmityl  and  oleyl-lecithins.  and  Thudichuin 
rofiards  it  as  pos.sil,le  that  two  difTereiit  fatty  acid  radicles  may 
enter  into  the  combination.  therei)y  increasinjr  the  numher  of 
possible  lecithins. 

All  of  th.M'  substances  occur  in  ;inimal  cells  in  abundance, 
and  their  decomposition  products  are  found  normally  in  traces 
in  the  urine."  but  under  abnormal  conditions,  particularly  in 
certain  metabolic  and  nervous  disturbances  with  toxic  .symptcmis. 
cholin  and  -lycerin  ior.i-ani(M  pho.sphori.-  acid  have  been  foun.l 
much  increa.sed  in  tho  urine.' ' 

The  second  -roup  is  made  up  of  nitrogenous  but  phosphoru.-- 
free  lipoids,  the  so-called  cereimKsides.  and  related  to  the  jjlyco- 
sides.  which  form  constituents  of  the  .so-called  prota^on. 

The  third  ;ind  very  important  j^roup  is  represented  by  the 
Mon-nitro-.'iiousand  iion-plu.sphorized  cholestcrins.  which  belon- 
to  th.'  terpenes.  T|„,s,.  ,,,-,.  „f  very  -reat  interest,  not  .,nlv  on 
.'•ec(.unt  of  their  wide  occurrence  in  the  animal  and  vegetable 
kinfrdoni.  as  the  so-called  phytosterin.  but  Ix-cause  they  par- 
ticularly have  acrjuire.l  a  very  -.vat  nMe  in  the  pr()i)lems  of  fat 
defeneration  .and  fat  infiltration.  The  elch-r  Beneke  drew  atten- 
tion to  the  abundant  (•ccurrences  of  cholesterin  nianv  vears  airo. 


DKiiKNKHATIVK    AM)   KXIDATIVK    NKI'HKITIS 


121 


hut  not  until  rocoutly  has  this  iniportaiicc  liccii  proiK'rly  valued. 
Chcinically,  it   has  the  formula  (VHu.O.  and  is  a  nionovalont. 
simple,  unsaturated,  secondary-  alcohol,  containinfi  four  saturated 
hydrated    miclei.     The    chemical    constitution    of    cholesterin 
stamps  it  evidently  as  c()mi)licate<l  terjHMie,  /.  «■.,  isomeric  hy- 
drocarbon of  the  <;eneral  formula  ('i,,!!,,,.     It  has,  therefore,  no 
chemical  relation  to  the  previously  mentioned  substances  or  the 
fats.     Related  to  the  cholesterins  in  the  animal  body  are  certain 
decomposition  products,  as  kaprosterin.  formed  in  the  <iut  from 
the  cholesterin  of  the  i)ile,  and  further  isocholesterin,  found  in 
lanolin.     Part  of  the  cholesterin  secreted  by  the  bile,  however, 
seems  to  be  reabsorbed  by  the  ;iut,  similarly  to  the  l)ile-pi<iment. 
.\s  an  example  of  its  wide  distribution  throu<ih  the  animal 
body,  I  mifiht  mention  that  it  apparently  forms  an  outer  z(me  to 
many  cells,  and  acts  antajionistically  to  cell  .solvents.     Tims,  in 
erythrocytes  it  is.  accordinji  to  Hanson,  distinctly  .so  to  the  hemo- 
lytic .iction  of  .saj«)nin."'     The  orifrin  of  cholesterin  in  the  body 
is  so  far  unknowti;  it  may  })o.ssibly  be  derived  from  the  vejjetable 
phytosterin.     Its  natural  history  in  the  body  is  also  unknown; 
liut  it  occurs  in  combination  with  fatty  acids,  and  particularly  as 
esters.     Protafion,  which  I  mentioned  l)ef()re,  has  had  a  very- 
disturbed  hi.story.     First  discovered  by  Liebreich  in  \H(\o,  and 
pronounced  an  •  ntity.  it  appears  now  to  be  mo.stly  a  mixture  of 
phosphorized  and  phosphoru.s-free  lipoids,  particularly  .sphyn- 
jiomyelin  and  phrenosin.     .V  protajion-like  sul)stance  occurs  in 
nephritis,  accordinj:  to  Lohlein'"  and  others,  in  crystalline  form 
in    the    intertubular   tis.sue   and    the    lymphatics.     It    is   there 
probably  derived  from  an  abundant  disintejiration  of  cell  proto- 
plasm.    It  is  doubly  refractive,  and  jiives  the  sudan  III  fat  stain, 
soluble  in  alcohol  and  in.soluble  in  acids  and  alkalis.     Panzer,"* 
however,  has  shown  that  this  is  probably  also  an  ester  of  choles- 
terin aith  fattv  acids. 


,1  < 
\ 


V2: 


ItliKiHT  S    DISLASK 


It  liMs  »lc\cl()|K'(l,  llicrcforc.  tli:it  f;it-n'l;ilt'<l  substances  may 
apiM-ar  iliiriiii:  the  (lisiiit(';j:iatinti  of  tlic  protoplasm  of  all  rclls. 
and  that  some  of  these,  on  further  decomposition,  mav  vield 
neutral  fat.  'iliis.  mider  such  conditions,  is  therefore  not  neces- 
sarily i)rouiiht  to  the  p.irts  from  distant  depots. 

Now.  what  does  all  this  re|. resent,  ;ind  what  is  its  relation  to 
fat  deucneration  .and  fat  infiltration? 

In  the  cours(>  of  investijiiition  into  this  problem  .some  very 
interestinu  jioints  developed.  i{osenfeld  as  the  first  drew  at- 
tention to  the  fact  that  the  inicroscopi<-  ap|M'ar;inces  and  valua- 
tion of  fat  contents  of  an  oru:in  .are  umcliable,  and  that,  there- 
fore, chemic.d  .and  morpholo^iical  results  do  not  cover  each  other 
in  fat  determination.  I!(>.ilth\  and  fatty  kidneys  m.ay  not  .show 
their  fit  contents  at  all,  even  if  this  amounts  to  '2'.i  |H*r  cent. 
.\|(»re  curious,  however,  is  the  fact  that  kidneys  of  the  same  fat 
contents  (  I7.*.>  to  IS. -J  per  cent,  i  may  apjw'arat  one  time  healthy, 
at  another  extremely  fatty.  Kidneys  with  even  a  diminished 
amoimt  of  fat,  say,  10  percent.,  may  .seem  to  us  at  times  extremelv 
fatty.  That  this  is  not  peculiar  to  the  kidney  was  .shown 
l)y  Bo.-<sard  and  Schmoll  .and  I{osenthal.'''  'I"he  latter  could  not 
demonstrate  morpholojiically  with  osmic  acid  and  sudan  any 
fat  in  cheesy  tuberculous  ma.s.ses,  while  ether  extracted  on- 
sid<>rable  .amounts  of  soap  and  cholesterin.  Ivlotz,-"  from  Adami'.s 
laboratory,  has  only  recently  pointed  out  that  at  least  part  of  the 
myelins  in  the  kidney  «>xist  as  soaps  of  oleic  acid,  and  that  su;'h 
fatty  compounds  are  not  readily  demon.st rated  l)y  the  ordinary' 
stainin;;  with  sudan  III.  but  can  l)o  obtained  by  extraction 
with  ah'ohol.  It  is.  therefore,  evident  that  the  pre.sence  of  fat 
and  fat-like  substances  may  not  always  be  visible;  on  the  other 
hand,  may  l)ecome  visible,  with  relatively  .small  quantities,  not 
expeedin<>;  the  normal.  From  the  forejioinj;  it  follows  that  the 
morpholofiical  ap{)earance  of  fat  in  the  orfian.s  means  not  neces- 


l)K«iK\KUAII\  K    AM)    K.M  DATIVK    NKI'IIIMTIs 


12:{ 


sirily  iiici«';i.s<'  in  f;it,  l>ul  :i  tiiolcciil.-ir  pliysicil  (Iccoiistitutiori  of 
the  cell,  \vli('tcl)y  f.it  <»iiv:iii:illy  coiilaincd  :iii«l  coiiccalcil  in  the 
stnictuiT  <»f  flic  protoplasm  :ip|M'!iis  fret'  to  lis.  Kraiis,  '  and 
particularly  Alhrcclit.-'-'  whose  ideas  I  have  already  presented  in 
coiincclioii  with  parencliyniatous  dejieneration,  assiiinc  for  its 
explanation  that  proto|)lasni  exists  iiornially  as  a  fluid  pulp,  an 
emulsion,  which  contains  fatty  siihstances  so  finely  divided  that 
they  are  invisilile.  !\  rails  draws  at  tent  ion  to  the  fact  that  neutral 
lluid  fat  does  not  reailily  emulsify.  Imt  does  so  as  soon  as 
some  f.itty  acid  is  added.  i'liis  is  expliiinal)Ie  liy  the  supposition 
that  fluid  fat  is  a  solution  of  f.itty  ;icid.  whose  molecules  ;ire 
e<|ually  distrilmtcd.  :is  in  all  solutions,  hetwicn  those  of  the 
neutral  fat.  If  this  mixture  is  hroiijrht  into  contact  with  an 
alkali.  the.s<' nioleculesdiffu.se  into  it  and  form  soaps,  which  unite 
as  a  honeycomh  (Biit.schlii.  inclosing  within  it  the  fluid  fat  in  the 
form  of  drops.  .Mhrecht's  "troptijic  llntmischun^."  or  myel- 
inic deconstitution,  wiiich  we  have  reviewed,  would  Ik'  of  a 
similar  nature,  althoujrh  it  also  includes  important  chanjies  in 
the  protein  constituents  of  the  protoplasm. 

'i'he  old  conception  of  Virchow,  who  spoke  of  a  direct  tran.s- 
formation  of  protein  into  fat.  has  l)een  discarded,  therefore,  and 
Kraus  has  reintroduced  the  term  fatty  metamorphosis,  by  which 
is  understood  a  physical  deconstitution  of  the  cell  protoplasm, 
with  the  lil)eration  of  fat-similar  substances. 

A  different  view,  however,  is  entertained  by  A.schoff.''  who 
still  rejiards  the  vital  fat  proces-ses  as  infiltrative  in  character. 
In  favor  of  this,  he  puts  forward  the  coexistence  of  i.sotropous 
and  anLsotropous  drops  in  the  same  cells,  the  oceurr'^'nce  of 
anisotropous  substances  in  cells  which  show  no  evidence  of 
dejieneration,  and  particularly  the  re.sorption  of  anisotropous 
drops  by  the  endothelial  lymph-cells  of  the  fjall-bladder  in  lonji- 
continued  bile  stasis;  he  holds,  further,  that  in  abscess  formation 


I- 

h 

|i 

:!  , 

it 
{ 


^^ 


IE 


:r 


r' 


I 


Il»l 


HHKMIT  S    I)1SK\SK 


:iii»l  (liiriiifi  «l(M;«-iicr;tliv»'  itifl:itnin!il(trv  lesions.  :is  in  loii^-con- 
limicd  lu'phtili.s.  clKtli-stcriii  is  s<'t  free,  .iiid  citlicr  rcphiccs  the 
v:lv((  rill  with  the  forni.'ition  of  li|M>i(|s,  or  is  t.-ikcii  up  l>v  cells  :is 
eoiiipleted  cliolesteriii  ester  with  other  iieutml  fat.  lie  therefore 
sjM'.iks  of  two  irroiips  of  fat  infiltrations:  one,  the  jrly<<'iin-<'ster- 
fat  infiltration,  .md  the  other  the  cholesterin-ester-fat  infiltration. 
.\scholTditrerenti;ites  these  chan-ies  definitely  from  the  .so-<'alled 
po.stinorteni  or  .•iiitolytically  orijiin.atinv:  myelins.  The  latter, 
he  st.'ites.  .almost  always  lack  .arii.sotropism  in  contradistinction  to 
the  intravit.il  forms.  They  .ire  not  f.-ttty  in  reaction,  and  then^- 
foH'  lack  the  chanicteristic  stains  of  these  suKstafices  with  sudaii 
III.  Sch.arl.ich.  Nilehhie.  and  osmic  .icid.  Hut  he  admits  that 
durinji  autolysis  fatty  .sul)stances  of  the  ;rlycerin  and  cholesterin 
tyjM'.  which  were  stored  in  the  cells  durin;:  vital  proc«'s.ses.  may 
apjM'.ir. 

There  .are  one  or  two  other  points  which  deserve  considera- 
tion. 

Uuhow-' showed  that  the  percent.'i^-c  increase  of  f.at  in  the 
fattily  de^renerated  he.trt  was  relatively  very  low  i.ti  per  cent, 
of  the  moist.  N  per  cent,  of  the  dry.  mu.scle  sul)stance.  amountinj: 
to  only  ;d)out  .i  |H'r  cent,  of  the  fn  sh  mu.scle,  not  more  than  ')  to 
S)  fim.  for  the  whole  heart.  Many  times  it  is  |<>ss.  These 
fiviures.  HuIm)W  holds,  cm  he  explained  |H'rfe<-tly  on  the  stren<rth 
of  the  norm.al  fat  contents  of  the  hlood  ((».!  to  1.4  |«'r  cent. ). 
which  have  not  been  normally  t.aken  up  l)y  the  injured  protopla.sm 
of  the  cells.  .\s  re.a.son  for  this  inability  of  fat  reai)sorption  liy 
the  cells  he  re;iards  diminution  of  alkalinity  of  the  pla.sma. 
Contributory  evid<Mice  to  this  view  m.ay  be  -rained  from  the  fac  t 
that  an  ini  rease  of  .icid  production  has  been  actually  noted  in 
conditions  that  are  very  .apt  to  be  a.s.sociated  with  f.itty  changes, 
and  that  fatty  acids  are  formed  din-in-;-  autolysis.  Hubow  al.-o 
rejrards   the   fatty   cell   as  an    injured   cell,   which,   under   toxic 


I)K<;K\KUATI\  K    AM)    KXt  DATIVK    NKrilHITIS 


li.') 


influences  aixl  :i  |>erv(>rt(><i  in(>t:ilH>listii.  pnxliK'cs  more  iicid  :iii(l 
|»n>h:ilily  discliMivcs  less.  As  ;i  result .  <liruinislie<i  .'ilkalinity 
(»f  the  ••ell  plasma  follows,  with  inaMlity  of  fat  al)sor|>tioii. 
Oswald"'  has  |M)iiite(l  out  that  the  ideas  of  Huliow  are  really  not 
o|>|M»sed  to  thos<'  <if  lios<>nfeld,  inasiiuich  as  it  may  Im*  su|)|>os<>d 
that  the  Idood  leaves  its  fat  in  the  dej;eneratin;;  organs  to  later 
carry  more  fat  to  it  from  the  distant  fat  de|Mits  of  the  Inxly. 

Now,  to  sum  up:  I'roiu  the  fore^oiny:  it  ap|H'ars  that  the 
oc<"urrence  of  fat  in  the  orjiaiis  is  not  of  uniform  character,  and 
also  not  of  uniform  derivation.  It  may  occur  first  as  a  tnmspor- 
tation  of  material  to  cells  for  the  purp<»s<'  of  supplyin<r  :tn  e.asily 
coml)Ustil)h'  suhstance.  or.  I  take  it.  as  a  compen.satorv  proce-ss 
tr»  relieve  a  loss  of  protoplasmic  parts  of  the  cells,  which  takes 
place  either  as  a  direct  destruction,  or  hy  '|Uantitative  inter- 
f«'rences  with  the  cell  nutrition,  as  durinji  inactivity  and  simple 
atrophy  of  orjians.  Whenever,  in  such  ca.ses.  restitution  of 
protoplasiiiic  inat(>rial  l«>comes  im|M)ssilile,  fat  is  sulhstituted. 
This  accumulation  is  aided,  undouhtedly.  in  many  ca.ses.  hy  in- 
ahilify  to  burn  fat  pro|H"rly.  The  nature  of  this  fat  is  largely 
neutral,  isotropous  fat  ^rlycerin  esters.  But  win  ii  this  proces.s 
liecomes  a.s.sociated  with,  and  takes  pla<r  under,  conditions 
leadin;:  to  rapid  cell  destruction,  it  has  added  to  it  anisotrojMius 
cholesterin  esters  and  other  lipoids  which  either  orij^inate  in  the 
cell  it.self  or  are  hroujiht  to  it  from  other  cellular  .sources. 

On  the  other  hand,  in  severe  defieuerations.  necrosis,  and 
autc»lysis  of  cells,  there  occurs  from  the  start  a  severe  internal 
revolution  within  the  protoplasm  of  the  cell.  Ieadin<i  to  jieneral 
liisorfranization  of  the  latter,  with  the  setting  free  of  fat-related 
substances;  these,  on  further  decom}M)sition  and  re-synthesis, 
may  later  jrive  rise  to  neutral  fats,  and  lead  to  fat  infiltration  of 
otlier  cells. 

Kat  infiltration  and  fat   metamorphosis  are  then  two  inti- 


u 


1 2() 


MHKIIIT  S    DISKASK 


niMtcly  coiiiu'ctcd  and  related  conditions,  wliich  deiKMid  eitlier 
on  the  existence  of  livinji  ceils  or  on  dead  or  dyin<>-  and  dis- 
orjianizinji  cells.  The  conii)licate(l  nature  of  nutritive  disturb- 
ances in  orjians  makes  a  conihination  of  both  of  these  at  times 
probable,  and  tlu  dimini.shed  alkalinity  of  the  blood  may  well 
be  an  infhiencinj;  factor. 

Under  normal  conditions  a  moderate  dejrree  of  fat  infiltration 
in  th(>  kidney  has  Ikhmi  noted  by  von  Haii.seniann,  and  we  can 
easily  conceive  of  this.  Hut.  on  the  other  hand,  the  myelinic 
disintejiratioii  of  cells,  and  the  occurrence  of  jM-otajion.  choles- 
teriii.  and  related  bodies  in  considerable  amount,  must  always  l)e 
of  j)atholoiiical  orijiin. 

Jieariiiii  in  mind  the  experiences  of  this  excursion,  and  to 
return  to  our  morpholonicai  considerations,  you  will  be  in  a 
position  to  appreciate  the  j-reat  individual  variations  wliich  the 
kidney  under  consideration  may  present.  The  fat  may  either  be 
recojinizable  in  patches,  streaks,  or  cover  lar<;er  areas;  it  may  be 
confined  to  certain  parts  of  the  tubules,  jiarticularly  the  loops 
and  proximal  end.  or  it  may  l)e  diffuse,  involvin<>  the  whole 
tubule,  althouiih  in  varyin;-  dejiree.  In  the  be-iiiiiiini!;  of  the 
process,  fat  appears  in  the  peripheral  portion  of  the  cell  near  the 
tunica  propria.  While  these  chanjies  are  more  prominent  in 
the  epithelium  of  the  tubules,  they  may  sometimes  reach  a  hifrh 
dejiree  in  the  iilomerulus. 

I  turn  now.  secondly,  to  the  further  events  which  take  place 
in  the  lilomenr'  and  tubules  subseciuent  to  the  infiatnmatory 
chaniics  with  which  we  have  already  become  actpiainted. 

In  the  jilomerulus  we  had.  you  renietnber,  dejicneration  of  the 
linin«i  epithelium  and  endothelium  of  the  tuft,  with  proliferation 
of  the  latter,  exutlation  within  it  and  into  the  capsule,  and  at 
times  i)roliferation  of  the  epithelial  cells  advaiicinji  from  the 
periphery   toward   the   center.     The  whole  tuft    l)ecomes  thus 


DEliENKUATIVE    AND   EXUDATIVE    NEPHKITIS 


127 


riH-  ;fO.  lliiih  iii;i)inific,iti(ifi  (if  (jlniiuriilus,  r-liovvinu  l"'''!"!!  inh  allied  lo  lliiit  <if  I'i(£. 
II.  The  tlallciicil.  tilirillar,  ■•apsuliir  cells  arc  seen  to  fuse  with  the  cells  of  the  atropine 
tnlt.     Kew  iirnisiiallv  large  capillary  loops  sliow  in  cross-section. 


DK(iENEKATIVE    AND    EXIDATIVK    NEPHRITIS  129 


t; 


■H 

T  '■ 


I'ig   :il.     Till'  wliiilc  ulohiili'  li.i-^  liccdiiH'  involved  in  a  liyalim   ininsforinalion. 


10 


l)K(iF.NKH.\TIVE   AND    KXIDATIVK    NEPHRITIS 


131 


KiK-  •(-■     roiiiplctcil  liyjiliiii'  transfoniialioii  of  si  Kloxicrolo^  «illi  (vw  imclfar  remnants. 
Surn)uniU'(l  1)V  very  oclliilar  filiroiis  tissue. 


DE(JENERATIVE   AND   EXUDATIVE   NEPHRITIS 


133 


imi)ermeable.  Inflammaton'  thrombi  form  within  the  capillaries, 
while  the  cellular  exudate  fuses  with  necrotic  cellular  material 
and  unites  the  capillary  lobules  of  the  tuft  and  the  capsule  to  a 
mass.  This  leads  to  several  results.  If  the  tuft  has  been  shut 
off  from  all  communication  with  afferent  and  efferent  vessels, 
it  necessarily  disintefjrates  rapidly,  so  that  its  parts  break  off 
into  frajiments  and  are  washed  away.  If,  however,  some  com- 
munication with  the  outside  vessels  has  lieen  retained,  a  rather 
irrejtular  destruction  of  the  {glomerulus  follows:  and  some  of  the 
still  permeable  capillaries,  particularly  near  the  hilus  of  the  slom- 
erulus,  underj^o  compensator}-  dilatation.  The  endothelial  cells 
of  these  capillary-  walls  swell,  while  those  of  the  collapsed  areas 
underjio  fusion.  Capillar\'  lobules  are  thus  obliterated  and  dis- 
connected from  the  still  permeable  portions  of  the  tuft,  and  fall 
to  one  side,  to  underjjo  rapid  disintejiration.  Finally,  the  whole 
of  the  tuft  filled  with  endothelial  nuclei  and  hyaline  masses  and 
some  leukocytes,  breaks  up  into  disintegrating  lobular  remnants, 
and  the  capsule  collapses. 

Where  the  capsular  epithelium  has  undergone  marked  pro- 
liferation, these  cells  liecome  flattened,  string}^  fibrillar  in  ap- 
j)earance,  fuse  with  the  other  cells  of  the  tuft,  or,  stagnant, 
retained  albuminous  exudate  to  hyaline  material.  It  is  pos- 
sible that  endothelial  cells  of  the  obliterated  tuft  may  take 
part  in  a  similar  fibrillar  and  subsequent  hyaline  transformation 
(Figs.  30,  31,  32).  The  destruction  of  the  glomerulus  and  the 
Malpighian  lx)dy  is  usually  not  so  violent.  It  may  result  from 
fibrinous  adhesion  of  the  capillar}'  loops  to  each  other  and  to  the 
epithelium  of  the  capsule.  Lohlein  considers  adhesion  by  des- 
quamated capsular  cell  detritus  sufficient.  Thus  immobilized, 
a  gradual  connective-tissue  synechia  of  capsular  connective 
tissue  and  glomerulus  occurs.  The  connective  tissue  grows  into 
and  separates  the  fused  glomerular  lobules.      Ziegler,  Engel, 


l.U 


KIIKiHT 


DlSKVSK 


and  Hrrxhciiiicr  have  drawn  aftcntidu  to  similarity  of  tlu'sp 
(•lianji<'s  with  tli<)S(>  observed  in  serous  inenihraiics. 

A<:ain  in  protracted,  less  l)rus(jne  cases,  the  ;rlonierular  loU's 
are  transformed  liy  hyahne  swellin<>:  (»f  the  loojis  and  eiidothelial 
and  possiljly  epithelial  proliferation  into  a  compact,  i)lump. 
first  cellular,  then  hyaline,  body.  Amyloid  material  is  deposited 
in  the  capillar)  loops,  particularly  in  constitutional  di.sea.ses. 
a.ssociated  with  hyaline  infiltration  of  other  orjraiis  and  vessels. 
According!  to  Wicliman  and  Martland.  amyloid  material  infil- 
trates the  parts,  wnile  the  cells  are  not  transformed  into  amy- 
loid, and  Hueter  finds  the  amyloid  dejK»site(l  within  the  lumen 
of  the  capillary  vessels.'' 

Other  j)rocess<^s  may  als<i  lead  to  hyaline  transfonnjttion  of 
the  .Malpiirhiaii  l)od>  ,  as  the  res\ilt  either  of  lack  of  pr()|)er  Mood- 
supply  of  the  glomerular  tuft  or,  as  l»onfi<-k  Itelieves.  as  the  result 
of  stajiuation  within  .and  ohliteration  of  the  convoluted  tuhules. 
In  such  events  the  epithelium  and  endothelium  of  the  tuft 
heconie  p;ile.  turhid.  swell,  and  fuse  to  a  structureh  .ss.  hyaline 
IxkIv.  This  is  occasionally  initiated  1)V  (edematous  iml)i)>ition 
of  the  parts,  so  that  the  }il<»"i<'"ilii^  'iUs  the  distended  c;ip- 
sule.  A  common  event  is  connect ive-tis.s\ie  invasion  from  the 
capsular  tunic,  which  pushes  before  it  ;i  «i'"a(lually  atro})hyin^ 
capsul.ir  epithelium  (  Fiji.  HSk  Accordinj;  to  some  of  Dr.  .Milne's 
observations,  this  seems  to  be  the  cast*  in  •ilomeruli  wliere 
oriiiinallv  the  exudate  lifts  the  epithelial  cells  off  tlu'  ba.sement 
membrane  and  pu.shes  them  bef(»re  it  toward  the  tuft.  I^ater, 
this  exudate  is  repl.-iced  by  gradually  thickeninji  e;ipsular  con- 
nective tissue,  which  occasionally  still  shows  toward  the  tuft  :i 
very  thin,  :ilniost  endothelial-like,  cellular  lining;  ( Fijj.  S  and 
riiis.  :il)  and  4(h. 

Similar  is  the  fate  of  the  ulomerulus  in  ca.ses  when,  as  we  saw 
iK'fore,  only  a  portion  of  the  tuft  has  In'en  firmly  attached  by 


DEOKNKKATIVK    AM)    KXIDATIVK    XKPHKITIS 


i:i." 


li(£.  ;!:i,  -In  one  uloincriiliis,  iiiflainnmliiry  nttaclunrnt  lo  rapsulc,  with  localiztHl  pcri- 
illoiiicriilar  tliickcninR;  incrcii.se  of  emiollirliiil  nurlei  in  l)<)lli  (jloineruli.  Diliitalion  of 
lapsulc.      X  1S5. 


DEiiKNEKATIVK   AND   EXIDATIVE   NEPHKITIS 


137 


Km.  34. 


-Various  Htaffioti  of  hyalint'  nlomonilur  rcplacpment. 

X  200. 


Hyaline  rmtts  in  tubules 


J  E 


KiR.  IC).— One  glomerulus  with  complete  hyaline  atrophy.     Hyaline  elianne  in  u  glomerulus 
eommeneing  in  the  part  attached  to  capsule.     X  "220. 


DKtiKNKK.MIVK    AM>    KXIDATIVK    SKI'IIKITIS 


i;j<j 


I  It   :Ui.— ('(inipli'tc  liyaliiic  filriipliy  of  :i  (jlnmcniluH.     In  tlio  iii'inliliorliiMiil  a  very  iiuicli 
tliii'kcnril  anil  iiliiiD^t  nlilifcralcil  vi's^d.      X  i(M». 


I  li;  :17       Vilvanip  1  filirous  iiu vision  and  rfplarrnHMil  of  a  (jlomcruhis.     An  ailjoinin(j  rela- 
tively licallliy  glomerulus  in  compensatory  funelional  hyiwrtropliy.      X  aX). 


DEGENEHATIVE   AND   EXIDATIVE    NEPHRITIS 


141 


-'•  -'^i^BuJ 

• 

« 

^^'  *i^ 


Fi(t.  :{8.  -Gnuiual  pcriphoral  fibrillar  invasion  of  a  liyaline  glotnorulus. 


DEGKNEKATIVK    AND   EXUDATIVE    NEPHKITI.S 


143 


Fi({-  •{'■•■  <';i|i>iilar  ihickcniiiK  vvitli  <'xt(•n^i(ln  of  lining  cells  bcfori"  it  iind  fibrous 
rc|>lacciii<'nt  frmii  an  attacliril  jioinl  of  tlii-  liasc  of  llic  tuft.  CompU'ti'  hyaline  transforma- 
tion of  a  Kl<"<ierulu>.     Some  of  the  tuhiiles  till<"<l  with  newly  formeil  cells.      X  'i°JO.f| 


Ki(f,  K).  — AiUanceil  anil  inva<liiig  fibrous  capMular  thirkeninR  of  n  Kloineruias.      X  'i'M. 


ill 
'11 


DE(iENKKATIVE   AND   KXLDATIVE    NEPHRITIS  145 


Fig.  41. — Now  cylindrical  epitholium  in  tubules  in  productive  nephritis. 


11 


DKOKNKKATIVK    Wr)    KXIDATIVK    NKrHUITIS 


147 


cxudato  to  a  part  of  tho  capsule,  wliich  is  usually  dose  to  the 
entrance  and  exit  of  the  vessels,  althoujih  it  may  occur  in  other 
parts  of  the  capsule  as  well.  Then  it  jrives  rise  very  soon  to  a 
fil)roi)lastic  pioliferation  of  the  connective  tissue  at  the  {X'riphery 
of  the  capsule.  Hut  this  is  not  only  confined  to  the  jierifjlonjeru- 
lar  tissue,  which  firadually  thickens  by  the  concentric  de|M)sit  of 
fibrous  tissue  layers,  hut  it  invades  the  adherent  tuft,  and,  <irad- 
ually  <rrovviny  into  it.  replaces  this  hy  slowly  maturing  fibrous 
coiuiective  ti.ssue.  .\s  an  end-result  the  jilotnerulus  has  afiain 
l)een  ol)literate(l.  It  is  interestiiifj;  to  note  that  tliis  fibrous  in- 
vasion and  replacement  of  the  fjlomerulus  take  place  from  the 
spot  of  adhesion  to  the  cap.sule  i  Fiji.  33).  The  connective  tissue 
in  the<tlomerulus.  however,  very  soon  suffers  from  the  same  nu- 
tritive disturl)ances  that  the  obliterated  tuft  ex|)erience(l.  and. 
therefore,  iM'comes  jjradually  transformed  into  homo<ieneous 
material  which,  by  fusion  with  the  remaining!;  tuft  structures, 
jrives  to  the  whole  fjlomerulus  a  characteristic  hyaline  appear- 
ance. I^arly  in  the  process  bands  of  connective  tissue  can  be 
.seen  to  jirovv  into  and  separate  hyaline  or  amyloid  masses  in 
fllomeruli.  This  hyaline  material  still  encloses  cellular  and 
particularly  miclear  remnants.  loiter  even  these  disap{K»ar,  and 
there  remains  a  dead-lookinji,  non-functionatin<t  fjlobule,  sur- 
rounded by  somewhat  l)etter  preserved,  usually  loose  and 
stretched,  connective  tissue.  This  capsular  connective-tissue 
tyjx*  of  filomerular  replacement  has  lately  l)een  particularly 
emphasized  by  Herxheimer'*  (Fijis.  33,  34,  35,  36,  37).  All 
t\|M's  of  fibrous  jilomerular  replacements  are  associated  with 
concentric  |)eri;ilomerular  connective-tissue  thickeninjr.  This  is 
rich  in  elastic  fii)ers. 

We  see  tluit  in  the  hyaline  transformation  of  jilomeruli  all 
the  oom})onent  structures  are  involved,  capsular  epithelial,  capil- 
lary endothelial,  capsular  fibrous  connective  tissue,  assisted  b\- 


14,s 


HKKillTS    DISKASK 


any  exudate  which  may  In-  present.  The  resultir)^'  hyaline 
hodies  are  of  dilVerent  coniijosition.  This  is  well  illustrated  hy 
van  (iieson's  stain,  which  jrives  to  the  coiuiective-t issue  hyalin<' 
a  distinct  red.  to  the  others  a  yellow  color.  .\ccordin<r  to 
Herxheiiner.  the  yellow  lilomerular  hyaline  under<ioes  jrradual 
resorption,  while  the  red  connective-tissue  hyaline  is  more  resis- 
tant. .\  late  resuh  is  calcareous  infiltration  of  the  ;:lomeruli  in 
my  experience  not  a  very  fre<|uent  process.  Hauni  has  drawn 
attention  to  the  fact  that  many  of  the.se  calcareous  small  nodules 
are  really  calcified  cysts,  of  which  I  shall  sjH'ak  later. 

Coincident  with  all  the.se  chanjics,  which,  as  you  ai)preciate. 
are  difTusely  and  very  unevenly  distrihuted  throu;rhout  the 
kidney,  jro  necessarily  marked  alterations  in  the  size  of  the;rl(>ni- 
eruli.  The  best  pre.serv(>d  <rlomeruli  very  soon  underjro  func- 
tional coni|M'n.satory  hy|««rtrophy,  the  tuft  enl;ir<ies  to  not  only 
till  the  capsular  space,  luit  to  .actually  stretch  it,  and,  therefoi-e, 
(■nlarjres  the  whole  .secret inf:  apparatus,  rnfortunately  for  the 
individu.il.  such  jrhnnenili  are  later  apt  to  Ix^  overtaken  l»y  the 
s.ime  fate  as  the  others.  The  .atrophying:  and  de<j:eneratin«: 
jilomeruli.  on  the  other  hand,  show  much  diminution  in  size,  and 
the  final  hyaline  renujants  are  u.sually  .smaller  than  the  healthy 
glomerulus. 

-Now.  the  tuhules  also  present  gradually  a  very  varie  1  jjicture. 
.\s  their  epithelium  under«!;oe.s  diffenMit  states  of  de};eneration 
and  de.s(juamation.  they  enlarjie,  and  l)ecome  filled  with  cells 
and  cellular  dehris,  leukocytes,  ivd  blood-cells,  and  hlood-pifj- 
ment.  .\11  these  may  fu.se.  as  we  .saw.  into  cellular,  hyaline,  or 
waxy  casts.  Fatty  ca.sts,  of  course,  iKM'ome  frecjuent.  (Irad- 
ually  these  mas.ses  are  pushed  ii\on}i,  stafinatinn  jXTmanently 
or  for  a  time  on  their  downward  way.  Thi.s  stajination  i.s  aided 
hy  inflammatory  ol)literati()n  of  lymphatics.  Proliferation  of 
the  epithelium  is  here  also  a  prominent  feature,  and  of  the  same 


l)K(iK\KUATIVK   AND    KXTDATIVK    NKPHUITIS 


149 


tyiM's  which  \v«>  met  iH'forc.  /.  <■.,  iiiflaiiiinaton-  and  rojtpnorativp. 
Iiifiammatorv  hyiH-rphisia  of  (>|)ith(>Huiii  occurs  most  ahuiulaiitly 
iii  tlic  loops,  im<loui)t(Mily  iKM-aiiso  the  stagnation  of  necrotic 
masses  irritates  and  demands  phajrocytic  activity.  In  the  con- 
voluted tul)ules  it  usually  remains  confined  to  the  tuhular  wall, 
and  leads  to  many  multinuclear.  larjic,  irregular  cells,  witli,  not 
infre(|uently.  fusion  and  overjirowth  to  multinuclear  <riant-cells 
I  Fiji.  <"»!.  This  proliferation  may  occur  l)y  mitosis,  l>ut  accordinjc 
to  my  oi»servations  l)y  far  most  frecjuently  l)V  amitotic  division, 
and  I  would  put  this  latter  down  as  the  rule  for  the  multiplica- 
tion of  renal  epithelium.  In  clear,  or  at  least  relatively  clear, 
tultules  the  epithelium  re<ienerates,  but  in  an  muisual  manner. 
This  newly  formed  epithelivun,  particularly  well  observed  in  the 
convoluted  tubules,  is  frequently  not  of  the  normal,  hijth,  di.s- 
tinctly  striated,  jiranular,  and  protrudinj;;  tyjie,  but  of  a  low, 
smooth  protoplasmic,  in  places  syncytial,  in  others  endothelial- 
like  formation.  The  lumen  of  such  tubules  apjjears,  therefore, 
nuich  larjier  than  in  the  normal  kidney.  Ajsain,  in  some  tubules 
the  epithelium  l)ecomes  hijih,  narrow,  and  distinctly  cylindrical 
(Fifis.  28  and  41). 

This  newly  formed  epithelium  is  of  }ireat  interest  and  im- 
portance, for  the  questions  of  the  cause  of  this  atypical  formation 
and  its  function  immediately  pres(>nt  themselves.  That  filandu- 
lar  cells,  when  their  environment  chanjies,  also  chanjje  their  type, 
is  not  a  new  or  isolated  occurrence  hei-e,  but  it  is  well  known  that 
in  the  sclerotic  lun<is,  for  instance,  the  alveoli  become  tubular, 
and  their  lining;  epithelium  culxmlal ;  the  same  conditions  prevail 
in  the  sclerotic,  productive  inflammations  of  the  liver,  and 
.Milne-"  has  .shown  that  the  so-called  newly  formed  bile-ducts  in 
the  cirrhosis  of  the  liver  repre.sent  in  reality  old  bile-capillaries, 
which,  under  the  influence  of  the  new  environment,  have  changed 
their  cell  type.     The  same  conditions  prevail  in  the  kidney,  and 


.')(» 


hkkjiit's  hisiASK 


the  iiiniicii.v  of  s<.  many  aii.l   varial.lc  coiKlitioiis  uliicli,  ynii 
:i|)|»n'cial<'.  cnirr  into  this  new  (•iivitoiiiiicnt .  accounts  in  no  small 
•  Icurcc  for  the  many  atypical  c«-ll  forms  which  we  (>I)s«tv«'  diirinjr 
the    inflammatory    hyiH'rplasia.     ritimatcly.    when    conditions 
••••••oiiic  mon-  s<.|tlc(|,  a  -cncrally  uniform,  althouj-h  morpholojr- 

ically  .litTcrciii.   regenerated  epithelium  forms  as  the  result  of 
more  iwrniaiient.  Iiut  clianiicd.  environmeni . 

<>f  -reat  practical  interest  is.  <.f  coiu'se.  the  ;issoci;ited  func- 
tional chaiifie  that  imist  -o  iiand  in  hand  with  such  ;,  morplu.h.^r. 
ical  transformation.  .\l.out  this  we  know  very  little.  Ixit  it 
seems  :is  if  c(>rt:iin  complic;it«'d  .-uid  ohscure  functional  chan-re.s. 
which  .ire  .always  ol.served  l.ite  in  these  nephrites,  mijrhf  possihiy 
l.e  traced,  not  only  to  the  intlanunatc.ry  involvement  and  ana- 
tomical rearran;:,.,,,,.,,,  of  the  parts.  i>ut  also  to  the  loss  of  nor- 
m;d  and  the  production  of  entirely  new.  secretin-;  cell  ty|M's.* 

1  shall  refer  to  these  matters  ajiain  in  the  discussion  of  the 
so-called   coiitractnl.  or  interstitial,  hetter  termed,  productive, 
nei'lnitis.  where  these  morphological  and  functional  chanties  are 
m(.st  prominent  .and  ch.iracteristic.     Consider.ahle  variations  in 
size  of  the  tul.ules  (,ecur.     Some  are  very  nuich  hi r<;er  and  di- 
lated, either  .as  the  result  of  functional  hy|M'rtrophy.  or  as  the  re- 
sult of  stoppa;re  of  cellular  mas.ses  with  stajrnation  of  fluid  ahove. 
Others  ajiain  apjH'ar  collap.sed,  and  atrophy  for  reasons  which 
we  will  presently  discuss.     This  leads  directly  to  the  cpiestion  of 
the  result  of  such  chaiifres  in  -lomeruli  and  tubules  upon  the 
kidney  sul.stance.     Glomerulus  and  tulnile  are,  as  you  appre- 
ciated, a  unit  fn.ni  the  .anatomical  and  physiolojiical  .standpoints. 
A  iH'nnanent  injury  to  one  will  nece.ssarily  involve  the  other. 
So  it  hapjK>ns  that  the  tuhule  who.se  filomerulus  has  iM'en  lost  in 
either  of  the  ways  just  de.scrilx'd  will  collapse,  atrophy,  and  ulti- 

n  /  l"''"  \T  '"•'■'' ''••""'"■^"•••'"•-I  i"  llii;^  inslilut,.  for  «,„»•  tin..-,  aii.l  rocntly  V.  UiMvr 
Iro  8^0;^  rulo.  "'  «'""'-"''--'"-'      »"t  it  ...  n-ully  „o,  h.  alUnfnM,„,. „,' 


I>K<iKNKH.\TI\  K    AM)    KXl  DATIVK    NKI'IIIIITIS 


I'll 


iiialrly  U"  lost.  On  tlu'  otlifT  Ijaiul,  ;i  lonji-coiitiiiucd  Itlockiiin 
of  the  tul)uU'  in  any  |M>rtioii  of  it.  and  ;)arti(iilarly  fn'tjuciit  in  th<' 
region  of  \\iv  l(M>ps,  citluT  hy  cHlular  masses,  dotritus,  and  ph- 
IH'cially  hy  finiily  attached  casts,  will  s(M)n  load  all  the  slru<'tun' 
alM»ve  the  point  of  occlusion  to  tin*  sanio  fate.  While  this  has 
loiifl  l)een  reco^rnized  as  ;i  factor  in  the  loss  of  kidney  structure 
in  the.>*<»  lesions,  it  Ins  n  ntly  In-en  particularly  emphasized  Ity 
I'onfick-"*  as  tin  important  cau.s<'  for  the  w.iste  of  parenchyma. 
Indeed.  Ponfick  ji'X'x  ?<«>  fi»r  :»^  <«>  i»>l<l  that  much  of  the  jjlonieru- 
lar  atrophy  and  V>ss  must  1k'  attrihutrd  to  a  Mocking  of  tlie  tu- 
l)ules  at  a  considerahle  di.stance  Ih'Iow  their  orijrin.  Then'  can 
Ik'  no  (pie.stion  that  lK)th  of  these  mechanical  factors  are  lar<iely 
responsihle  for  the  «:radual  hut  projire.ssive  loss  of  substance, 
l)ut  they  an-  much  aided  in  it  hy  the  n'sults  of  the  inflammatoiy 
condition  in  the  intertuhular  suhst.-uice.  whicli.  hy  ohliteration  of 
lymphatics  and  capillaries,  wriously  interferes  with  the  mitrition 
of  the  parts,  'inese  I  will  consider  in  a  moment.  But  1  "fore 
doin^  .so.  it  mu.st  In*  appreciated  that,  as  a  result  of  this 
irrejiular  loss  of  substance,  the  kidney  now  l)e<rins  to  .show 
areas  of  collapsed  parenchyma.  l)etween  Ijetter  presei  vd  and 
even  swollen  parts.  The  surface  Ix'comes.  therefon>.  projjres- 
sively  sliffhtly  irre;j;ular,  puckered,  and  this  ap|M'ars  primarily 
and  more  prominently  in  the  cortex.  At  this  jH)int  the  cai)sule 
still  jH'els  rather  easily.  However,  this  loss  leads  now  to 
certain  other  chanjjes,  which  alter  still  more  the  ap|K»arance 
and  anatomy  of  the  orjian.  They  take  their  orifjin  and  pur- 
sue their  development  particularly  in  the  intertubuhir  tissue, 
and  spread  in  a  streaky  and  later  diffuse  fa.shion  throufihout 
the  whole  or^an.  We  nnist,  therefore,  proceed  ii"W  to  <onsi<ler 
the  fate  of  this  intertuhular  tis.svie  from  the  time  we  left  it  in  the 
process  of  defjeneration  and  exudation.  The  fact  tliat  lym- 
phatics and  tissue  spaces  are  here  not  cleared,  but  contimie  to  l)e 


l.-i2 


|ll!l<iin'>    l>l>K\^K. 


Mo.krd  Willi  fiitty  .iiiil  cclliiLir  iiimsscs.  while  the  infl:iiimi!i»(»ry 
u'dcniM  cnnliiiiH's.  N-.ids  very  soon  to  Idss  of  these  celhiljir  el«'- 
meiits,  followed  l>y  :i  |trolifei;ili(.ii  of  etidotheli;d  cells  within 
tlu'se  iliMliliels  ;md  the  ;ip|H'ar!iliee  of  lymphocytic  i  poly  I. hist  ic, 
h'ukocytoid  :iiid  lil.iol.l:istic  i-ells  without  The  cells  thus  pro- 
duced .lie  pMitly  |th;iuocytic  :iiid  partly  reconstructive:  licit  is.  ;i 
ceii.iin  nuinlM«r  ;iid  in  clejirinu  the  p;ith  for  the  development  of 
lii>rolil;istic  cells.  While  this  is  primarily  confined  to  the  inter- 
tuhular  sul».st;mce.  and  local,  it  soon  assumes  ^trealer  iliinensicms 
in  all  areas  where  adjoininii  tuhules  and  ;rlonieruli  are  wasting 
and  atrophied.  It  stands  to  rea.son  that  this  thickeiiiiii:  and 
((Iditeration  of  the  diaimels  of  nutrition  and  n-ahsorption  must 
also  interfere  with  the  tulmles  and  j-htmeruli.  .so  that,  in  my 
opinion,  thes<'  two  chaiijies  interact  and  <:o  hand  in  h.md. 

.Now.  as  the  HIiroMastic  cells  matun-,  the  intertuhular  con- 
nective tis.sue  hecomes  less  cellul:ir.  hut  thicker,  and.  by  rephice- 
ment  of  atntphied  parenchyma,  hands  of  comiective  ti.ssue 
(h'velop  leadin;:  to  more  (»r  less  firmly  contracting,  scars.  Hy 
jrrowth  on  the  surface,  the  capsule  U'comes  now  irrejiularly  .id 
herent.  so  tiiat  it  can  he  removed  only  with  ^^reat  difhculty.  and 
usually  takes  ,som<.  ,,f  the  parenchyma  with  it.  As  tiiese  chaiijies 
:ire  most  pronounced  in  the  cortex,  this  .suffers  the  mo.st.  It 
becomes  very  irrej-ular,  jinmular.  cicatrices  divi(h'  Iwtter  pre- 
served areas,  .md  the  normal  markin;:s  have  almost  entirely 
disapiM'ared.  <i\\\u<i  way  to  a  l.iz.arre  ;irran,<rement  and  mottled 
appe.anince  which  varies  much,  and  deix-nds  largely  upon  the 
coiKlilion  of  the  v.iscul.ir  .-ipparatus  i  I'iji.  42i. 

Occasionally,  hut  iiol  fre(|uently,  the  coniu  ili\e-ti.ssue  for- 
mation is  very  ditruse.  without  foim.ilion  of  thick,  contractiiif: 
scars;  the  surface  therefore  k mains  >ni(M.th,  althoujih  the  kiihiey 
shrinks.  Both  types  are  now  reco^inized  under  the  name  of 
secondary  contracted  kidnev. 


I)K<i 


liATIVK   AND    KXIDATIVK    NKI'HKITIS 


ir)3 


As  the  coiK  .  n  of  the  viiseuhir  apparatus  is  of  much  coiist"- 
(luence  in  the  fate  and  apjx'aranee  of  such  a  kidney,  we  must 
now  pay  some  attention  to  it.  The  vascularity  of  the  kidney 
(hirinj:  the  process  of  such  a  nephritis  n>ay  l)e  influenced  in  two 
ways:  first  and  directly,  hy  inflaninuitory  chanftes;  second  and 
indirectly.  I)v  chanties  in  the  general  circulation,  whii'h  result 
from  the  effects  of  the  nephritic  lesions  on  the  individual.  We 
have  s(H'n  In'fore  how  in  certain  inflammatory  lesions  the  affinity 
of  the  toxic  excitant  is  particularly  found  and  accentuated  in 
the  1  )Iood-vessels :  al)undant  dia|)edesis  of  red  Mood-cells  occur, 
hcmorrhafjies  and  even  extensive  hemorrhajric  extravasations. 
.\s  a  con.seijuence.  the  kidney  irddens.  either  diffusely  or  shows 
hemorrhagic  dots  and  streaks.  corres|K)ndinf!:  to  hemorrhajric 
extravasations  into  the  jjlomeruli  and  tuhules.  In  others,  ajjain, 
the  dejtenerative  lesions,  fatty  metamorphosis,  seem  to  empha- 
size that  there  the  irritant  effects  a  primary  and  jjreater  injurv 
of  tlie  fixed  tissue-cells.  In  thes(>  cases  the  orjran  appears  pale 
and  yellow.  Fmally  an  onlematous  iminhition  in  some  forms, 
particularly  those  associated  with  general  (edema,  may  fiive  to 
the  kidney  an  almost  colorless,  hut  moist,  ap|)earance.  The 
kidney,  therefon\  shows  here,  as  in  other  nephrites,  the  evidences 
which  |H»int  toward  one  or  the  other  inflannnator>-  attributes,  or 
i»oth  may  l)ecome  comhined  to  alx)Ut  an  etjual  dejrree.  In 
addition,  the  vascularity  must  Ik*  influenced  by  the  infiammator}- 
:inatomic:d  changes  in  the  architecture*  of  the  kidney.  Wei^ert 
w(  lit  .so  far  as  to  hold  that  the  (luaiuitative  differences  in  the 
Mood-supply  and  infliinunatory  enfiorsrement  of  the  ves.sels 
accounted  fully  for  the  diffei-ent  ap|K\arances  of  these  various 
forms  of  nephrites,  an<l  did  not  n'cofinize  them  as  inde|)endent 
lesions.  Other  invest i<:a tors  have  endeavoivd  to  establish  a 
definite  hemorrhafiic  nephritis,  distinct  from  the  .so-called  larmc* 
pale  kidney.     That  there  is  no  es.s«>iitial  difference  M'tween  thes«' 


ir)4 


HUKiHTs  r)isi  Asi; 


vmHoiis  fyiK's  u.-.s  illusti-MtcMl  vciv  f(ucil.ly  to  ..,(>  oi.lv  n-cci.tly, 
when  I  fouii,!  .•.  typic;,l  hn-c  licnioiTliMjric  kidney  „i,  the  loft  si.l'c! 
.'11(1  :.  siiuilMily  typi,:,!  l.-.r-r  pnlc  kidney  «.n  the  ri-ht  side,  of  a 
yonn-  -rirl  wl...  died  „f  ...  .^h.wjy  projrivssin-  nephritis.  It  ap- 
IH'.-ired  to  the  unknowin-  as  if  these  two  p,.rfeet  examples  ean.e 
from  diHerent  ind;-.  idiials. 

It  has  U'cn  claimed  In  some:  K.ieJK.hls  and  his  tV.ihmers.  who 
.•idvis<.  derapsulalion  of  the  kidney  in  nephritis,  that  with  the 
attaehment  of  the  .-apsnle  to  the  parenchyma  collateral  circula- 
linn  with  the  snrroundin-  sirnctures  may  thns  l«>  estahlished, 
i'Ut  extensive  experimental  ohs<>rvations  of  Theleniami.  von 
'■•'><■  •"'«l  Ilcrxheimer  ami  Hall,-"'  and  others,  have  shown  e<m- 
"Insively  that  this  .loes  n.)t  take  place,  and  after  decapsuhition 
.1  new.  much  thicker  capsule  is  soon  f<.rmed. 

S..oner  or  later  the  kidney  heuins  to  ex|M.rience  the  etTect  of 
tlH-  nci'l'Htic  proc-sson  the  whole  cin-ulation.  I  will  not  discuss 
Imtc  these  effects  on  the  h.>art  .and  vessels,  which  iK'k.njr  to  the 
last  chapt..r  ..f  these  |ectur<-s,  l>ut  it  is  particularly  to  the  com- 
pli<Mtin-r  pictures  which  venous  stasis  produces"  in  suc!i  late 
nephritis  that  I  wish  to  c.ill  your  .attention. 

Wnous  st.asis  in  the  kidneys  ;,s  the  result  of  ;,  -,.,,,.,..,1  ,|,.,.|i„e 
in  the  circul.ition  in  nephritis  m.iy  occur  rather  earlv  in  the 
lesion.  JK'fore  second.ary  atrophy  :,n,i  c<,ntracti<.n  have  t.ak.'U 
Pl.-"'<"-  <"•  l-'t<'.  Mfter  this  has  nnicl,  advanc.l.  In  either  .a.s,.  it  is 
••'P'  t..  .•onsideral.ly  modify  tj,,.  pro.-ess.  .and  to  \viui  to  very 
'■"'"'•'''"'"'''  •"'••'t'""i«"«l  .•nid  clini.-al  pictures.  If  the  circulation 
lH.c.»mes  impain'd  U-fore  mu.-h  ..f  the  kidney  sul.st.ance  h.is  Ikhm. 
l<»st.  the  veru.us  .'n-or-enK'nt  m.iy  prvvent  .at  le.ast  a  m.arked 
•'•.ntraction  <.f  tlieor-..n  alt<.jiether.  an<l  is  sometimes  re.sp<„.sil,le. 
I  Lelieve.  for  a  rem.-.rk.il.le  -ood  jrn.ss  preservation  in  th.-  size 
of  the  kidney.  Tlw  (|i.stril.uti<.n  of  the  l.lood-ves.s<.|s  acc.>unfs  for 
the  fact  that  the  st.asis  appears  first  and  is  Inst  m.irke.l  at  the 


I)K(;k\kh.\tivk   and   KXIDATIVK   NKIMIHITIS 


l.j.j 


junction  of  nicdiilla  and  cortex.  Therefore  the  lino  of  doniarcii- 
lion  iK'tvvccn  lioth  U'conics  more  pronnn(>nt.  Later,  the  inedulhi 
shows  accentuation  of  its  vess<>!s,  which  liave  usually  l)een  much 
better  prcM^rved  tlian  those  of  the  cortex,  and,  finally,  the  re- 
niaininiir  chaiuiels  in  the  cortex  also  l)ecome  more  prominent. 
Hut  as  these,  as  well  as  the  {ilonieruli,  have  larjiely  l«'en  lost  in 
the  intlainniatory  process,  this  is  relatively  less  conspicuous. 
\\  hile,  then,  the  kidney  as  a  whoh*  feels  fuller,  is  en<ior<j;ed  with 
Itlood,  and  denser,  this  occurs  n'latively  at  the  expens<>  of  the 
cortex,  Ix'iiiii  :it  ihe  same  time  most  prominent  in  the  medulla. 
After  venous  stasis  has  exi.sted  for  some  time,  it  leads  to  (edema 
atid  hemorrha^(>s  into  tuhules. 

In  the  projrre.ss  of  the  lesion,  if  the  individual  (htes  not  suc- 
luml).  which  is  usual,  it  is  difhcult  to  separate  the  effects  of  the 
stasis  from  those  of  the  nephritis.  :is  tluMpiantitative  and  (|Ualita- 
tive  conditions  iH'coine  well  .-ind  completely  interwoven.  Where 
the  Mood  .sta;;nation  is  marked  and  |)atchy  extra vasiitions  occur, 
ha-molysis  withsettiiifi  free  of  lilood  coloring-matter  and  precip- 
itation of  jiranular  pi<rment  in  .su<'h  affected  areas  takes  place, 
The.s*'  suf)enidded  nutritive  disturbances  an^  an  a(hlitional  cause 
for  patchy  atrophy  and  coUap.se  of  certain  parts,  while  others 
show  com|H'nsatorv  stretchinji  and  fullness. 

Clinically  svich  advanced  cases  pn^sent  jireat  diajinostic 
olist.'icles,  on  account  of  the  neces-sarily  complicated  fun«"tions. 
These  cases  are  fn'cpiently  very  difficult  to  .separate  from  lonp- 
contimied  simple  stasis  with  failiiifi  heart,  and  the  (|uesti(m  of 
<ieterminiiij:  whether  we  have  primarily  a  heart  lesio!i  with  pro- 
irre.ssive  vc'iious  stasis  or  primarily  a  nephritic  lesion,  which  has 
led  to  circulatory  disturbances  and  a  secondary  venou.s  con^e.s- 
tion,  may  l>e  iinjMKssible  to  solve.*     In  hospitals  which,  like  ours 

•  rriifcsNor  .S'li.ihir  liii.«  (old  iir  llmt  'rriiiilM'  uscil  to  |)ii\  [liirliruliir  iitti'tiliiin  to  tho 
ciilcir  ipf  till'  iiriiii'  ill  such  citscs.     In  vt-tKu-  siiLsis  I'liinpIicHliiiK  »  iii'pliritis  tin-  color  rc- 

Mmill>  pull'  ill  ipitr  of  ll-s.«'llnl  '|imillilv 


m 


14 


i.v; 


uKUiin's  insK\sK 


'City  Hospit.-.l.  \,.\v  V,.ik'.  receive  M  br-e  lum.her  cf  I l.esi' .•.<!- 
v;mce.l  c.ises.  some  jilriiosl  inoriluiiid  (.11  arrivjil.  they  are.  as  yon 
know,  more  or  less  naively  classi-d  as  cardii.renal,  \vlii<-li  leaves 
the  ultimate  diaj-iiosis  to  the  pathologist.  While  this  is  not  a 
very  scietitific  (.r  (>veii  definite  diajriiosis,  I  helieve  that  such 
••liiii.al  dia-iioses.  althoii-h  praetieally  eonf.ssiiijr  ifrtiotaiice.  are 
'•"tter.  for  the  sake  of  relial.le  stati.sties.  than  an  elahorat- 
aiitemortem  anatomical  dia,i.iio.sis.  which  cannot  he  controlled 
l)y  autopsy. 

Now.  (.n  the  other  Inn.l.  venous  sta.sis  may  not  occur  until 
late  in   the  .lise;..s...   and   after  .secon.h.ry  c(.ntraeti()n   has  well 
adv.-.ncfMl.      While   it    follows,    then,   the  -eneral  c<.urse  I   indi- 
cated, it  necessarily  ap|H'ars  much  m<.re  irre-ular.  particularly  in 
the  cortex,  where  many  of  the  vascul.ar  paths  have  l,e(Mi  either 
entirely   lost   or  ol.literated.  and  distorted.     The  kidney  in  all 
thes<.  c;,s«>s  loses  much  of  its  pale  or  yellowi.sl,  coh.r.  and  a.ssumes 
a   dark<>r.   cy.motic  ap|)<.ar.mce.     The  su|M'rficial   veins  ap|K>ar 
I)roininent.      Mere,  as  in  ordinary  stasis,  cyaiio.sis  is  accentuated 
in  the  medulla,  and  nnist  not  Ih'  conf(.unded  with  hemorrhajric 
inflammation  or  inflamm.itory  .•xa<-erl.ation:    thes<'  are  alw.-ns 
"lore  pn.minent  in  the  cortex.  .ukI  never  lea<l  t<.  dilatation  of  the 
larjier  veins.      They  m.-iy.  however,  comhine. 

I^istly.  to  sketch  the  fimctional  evidences  which  correspomi 
fo  the  morpholojrical  chancres  .sttidie,!  in  this  lecture:  When  you 
'•..nsider  the  multitude  of  interacting.  <-onstanfly  varying  proc- 
e.ss,.s  which  are  here  involved,  and  the  time  over  wliich  thes<' 
.'xtend.  with  the  po.ssil.le  compli.-ation.s,  I  think  y(.u  will  appn-- 
•  late  lh.it  similar  an<l  sometimes  very  complex  and  |KT-plexin>: 
functioti.il  corrolarij's  will  jro  with  them. 

.\s  Ion-  ;.s  the  proce.s.s,>s  of  exud:ition  an<l  defieuerat ion  con- 
trol the  fi.'Id.  th..  amount  of  urine  is  diminished,  althou-h  on 
iieeount  of  the  less  l,rus,|ue  process.  .ukI  com|M.nsat<.ry  action  of 


nKCiKNKUATlVK    AM)    KXIDATIVK    NKI'HHITIS 


i:.7 


|in"S('rv<'(l  <rl<tni('nili,  it  is  somewhat  larircr  in  (juaiitity  than  in 
the  scvorc  (IcjiorM'rativc  and  exudative  nephritis  invest ijjated  in 


our  first  lecture  lusuallv  uImhU  ")(Ml  c.c 


For  the  same  reason 


ilood 


is  not  apt  to  Ik*  presen 


t  in  lar":e  amounts,  and  the  urine 


Mpjx'ars  therefore  Hjrhter  in  color,  particularly  as  the  normal 
colorin;r-matter  of  the  urine  is  not  secreted  in  the  usual  (|Uan- 
til y.  Serum-all )umin  and  inicleo-all)Uinin  are  present  in  consider- 
alile  (juantities,  the  former  from  ().')  to  2  |K>r  cent.,  hut  only  rarely 
more,  and  the  hi^rlu'r  |K*rcenta<:es  rejKjrted  refer  to  those  of 
volume.  The  urine  is  ver>-  rich  in  morphotic  elements,  and  as  the 
fatty  dejieneralive  feature  U'comes  now  marked,  its  evidences  are 
ahundant  in  the  microscopic  examination  of  the  scnliment.  Katty 
cells,  fatty  casts,  free  fat.  and  detritus,  altove  all  others,  ^ive  the 
le.sion  a  characteristic  stamp  as  fatty  nephritis.  Where,  in  ad- 
ditioti.  liemorrha^res  (x-cur.  the  blood  apjK'ars  in  the  urin<'.  hut 
not  with  the  same  con.stancy  or  ahvmdance  as  in  the  more  active 
lesions  |)reviously  con.sidered.  As  the  process  proceeds  and  the 
exudative  featun's  n'}>n*ss  jrradually  to  the  hackjiroimd.  which 
.illows  the  field  to  l)e  somewhat  cleared  aJid  su|)ers(Mle(l  hy  the 
.(trophy  and  loss(»f  the  tissue  with  productive  cicatrizinji  chanjres, 
the  functions  .show  correspondinjr  changes.  The  amount  of 
urine  rises;  it  iK'comes  paler  and  clearer.  The  .sj)ecific  <i;ravity.  on 
the  other  han<l.  is  lowered.  lH'caus<'  the  excretion  of  normal 
solids  is  not  improved;  the  amount  of  serum-alhumin  and  mor- 
photic elements  is  dinunished.  Finally,  when  the  proce.ss  of 
s«'condary  contraction  is  well  under  way.  with  relatively  free 
paths,  and  the  jilomeruli  larjiely  ohliterated  and  non-function- 
atinji.  the  evidences  of  the  previous,  or  still  existinji,  exudation 
are  usually  slijiht,  hut  the  urine  surpri.sinjily  larjie  in  (luantity 
and  nnich  clearer,  almost  watery,  and  of  low  s|>ecific  jrravity. 
This  increa.se  in  amovmt  of  urine  is  usually  coincident  with  a 
decided  diminution  in  the  jii'iieral  (rdema.  which,  as  you  know. 


l.-)S 


u;ti(;iiT's  i)isi:.\>;k 


IS  most  alw.-.ys  very  innrkcl  .luriiij:  tho  .v.rlv  stM^os  of  this 
"•'Pl'ntis.  ...mI  whirl,  w,.  will  tnorc  fully  .lisniss  in  the  iioxt 
l<'<>""<'.  All..m.i.i  Mixl  inorplmtir  ..|,.nu.|.ts  .lin.inish  rmw- 
s|...n.hi,;rly.  (),H.„.ust  Ik>  .•...rrfnl  to  ,.ot  r.-.-,n|  this  fn.,,,u.„tlv 
••'l"«l|.l  .m,!  |M.r,,|,.xim  .I.T,.iff„|  rh;,t.-...  sotMHinu-s  .•.ssoriafil 
with  :.  t..,.|M.j.^  of  rHiof  <M.  the  p;„t  of  the  pati,.|,t.  ms  o,„.  for  th.' 
I'<''t,.r.  If  you  h,v,.  .•Mn.f.illy  f„|!„„,.,|  what  I  ,m.sr..t,Ml  t<.  vou 
''•■'•<'  KMl.iy.  you  will  l.rii.K  tlH..s<>  ovidciH-cs  i„  pro,H.r  n-L.tioi.  to 

'''••H.orplH.|,,jri,,,|H,ai.ji('si.H-i<lc.i,t  f(,tlH' pr(.jrr,.ss..f  th(Mlis(.;.s... 
."'<l  .idmit  no  ivpair  ,.r  iinpfi.voiu.Mit.  In  n-nlitv.  we  :.tv  (h-:.lii..r 
with;,  fuithcr  :„lv,Mir..  in  the  h.ss  of  tvunl  sul.slaiurs  aiul  sufli" 
••i<'M<y.  ai.oth<Tst.-po„  thclownward  road  to  the  fatal  tmnii.a- 
"""•  i'hv  h.st  is  fr...,u,.utly  hast,.u,.,|  l,y  au  .'Xarcrlmtion  of  tho 
••xu.h.tiv,.  and  d.-,.n,.rativ(.  pr...-,.sM.s.  Then  the  kidncv  presents 
.'UMUi.  as  nnich  as  it  is  al.l<-  und.-r  Ih,.  .•han-.-d  .-onditions.  th.'s,. 
various  anaton.iral  an.l  fun.tional  features.  Muf  it  is  |H,ssil,|,. 
'•';'»  ■•".  iri.livi.lual  may  survive  o.KM.r  even  more  of  these  exaeer- 
l>ations. 

On  lh<>  other  han.l.  when  venous  stasis  iK'coines   manifest, 

this  ,sres|H.nsil,le  for oth.-rsuiHTaddedfunetional  derangements! 
Ih-n-  als<.  the  urine  diminishes  ajr.-iin,  hut.  eontrarv  t(.  the 
'""••'""natory  exaeerhations.  does  n<.t  l.-a,!  toa-reater  all.umi.,- 
"na  than  fortnerly  exisfd  or  to  an  in.-tvase  in  morplu.ti.-  ele- 
ments, l-at.-r  a  relatively  small  a<lmi.xture«»fl,!,„„|-,.ellslK.eomes 
•'v.dent.  I.iit  the  .-olnr  of  the  un„,.  n'lnains  pale.  H.^o^nition 
•""'  '••'•■""•"  "f  this  .on.pheation  to  the  nephriti.-  pro<-e.ss  mav 
at  tim<'s  Ih'  difhcult. 

I  eannot  leave  this  di.seus.sion  without  at  h-ast  mentioninj:  cer- 
tain relat.-d  ki.lney  ehan«..s  whirl,  develop  late  in  primarv  .•hmnir 
venous  .onirestion.  an.l  not  as  the  re.sult  of  ....phrilie  hvsions.  Vou 
oi.derstan.l  that  fr..,,uenlly  i„  ,|i.s<,,.s<-s  <,f  th.-  h.-art  with  -ra.lual 
faihnjr    eomiM.u.salion.    lon--conlinued    venous    ,-on-estion    will 


I)K(iKNKHATIVK    AM)    KXIDATIVK    NK.I'UKITIS 


I.V.) 


occur,  without  any  previous  iiiHaininatioii  of  that  ornan.  Hen" 
all  the  veins  Imm-oiiic  monnously  and  projjn's.siv<'iy  on^orned. 
first  in  the  nirdulla.  later  in  the  cortex,  until  the  ennorjienient 
even  atTects  ^h)nieruli  and  arterial  v<'ss<'Is.  The  kidney  eii- 
larjres,  lK>con)es  extremely  rich  in  Idood,  an<i  its  inarkinv;s  very 
prominent.  loiter,  it  assumes  a  more  diffuse,  cyanotic  ap|)<»ar- 
.iiice.  As  the  n>s\ilt  of  the  mechanical  pressure  and  interference 
with  nutrition,  serum  will  transude  into  the  intertultuhir  tissue. 
The  kidney  apjH'ars,  then'fore.  in  later  .stajies.  (edematous,  and 
the  interstitial  ti.ssue  stretched,  homojjeneous,  :»nd  fihrillated,  es- 
pecially in  the  medulla,  whih'  the  tultules  are  relatively  eom- 
pres.sed.  Later,  I»I(mmI  extravasationsoccur  into  tubules,  and  sj'c- 
ondary  luemolytic  chan«r«'s,  with  .settinji  free  of  l)l(MHl-pi^ment. 
The  latter  is  particularly  well  shown  in  the  };lomeruli.  Now,  as 
the  result  of  these  larjiely,  and  primarily  (piantitative.  chanjjcs. 
atrophy  of  ;;h)meruli  and  tubular  {M)itions  occurs,  followed  by 
collapse  of  kidney  sul).stance.  In  such  areas  cellular  lympho- 
cytic ami  fibroblastic  ma.ss<>s  may  accumulate,  leading  to  mon* 
or  less  prominent  fibrous  tis.sue  jirowth.  As  a  result,  the  kid- 
ney .shrinks  and  contracts  in  places,  and  the  surface  apjx'ars 
necessarily  mon'  co.arsely  jrranular.  When  tubules  have  Ijecome 
cut  off,  cy.st  formation  may  take  place  under  such  conditions, 
particularly  in  the  ni(>dulla.  This  kidney  has  Ikhmi  deseril>ed  as 
cyanotic  induratioti,  or  cyanotic  contracted  kidney, and  is, .strictly 
.s|M'akin>i.  not  of  an  inflanmiatory  ty|H>.  It  di(Tei-s  from  the 
inflatiunatory  lesions  in  the  evidences  of  its  extreme  cyanosis, 
associated  with  ;:eneral  (edematous  imbibition  and  ma.s.sive 
prominence  of  the  larger  va.scular  channels.  This  state  of  affairs 
never  reaches  e(|ual  uniformity  of  distributi(»n  or  the  .same  di- 
men.sions  in  a  .stasis  which  is  engrafted  \\\xm  a  previous  nephritic 
lesi(»n.  The  contracti(»n  of  the  or«ian  in  the  cyanotic  induration, 
on  the  other  hand,  d(M's  not  ever  ac(|uire  the  pro|)ortions  often 


f  I 


m 


'*'**  HHKiin's    DISKASK 

si'vu  in  tin-  iiifl;imiii:it(.rv  |min'.ss«.s,  hut   \h(>  kidney.  :iltli()Uj:li 
••o;irs<'ly   -:ninular.    ivrn:iins   hrm^.   ;,iul    the   innlnlL-iry   jHirtiori 
particularly  pri.miuciit.  Inilliitiv:.  aiitl  the  cortex  never  excessively 
scarred.     Microscopically  characteristic  an-  ahserici-  (»f  marked 
•  leycneralions.  or  <"vidences  of  old  o,-  recent  cellular  exudation. 
This  is  particularly  well  shown  in  the  jilonieruli.     The.se,  althou^rh 
iinnien.s,.|y  <.nvM,iir,.,|  with  hlo<Mi  .uid  .soin.-  e.sca|M'  of  .s<.ruin  into 
the  capsular  space,  with  occa.sionid  adhesion  of  the  tuft   to  the 
s;iine.  do  not  present  any  features  of  active  exudation,  nor  that 
ireneral.  cicatrici.-d.   :ind  hyaline  repla.-enient   which    formed   .so 
|>romiiient  .1  feature  of  the  inflanunatory  conditions.     IVn.s*.  jH'ri- 
ulonierularcelhil.ir  infiltrations  .md  fihrous  ti.ssue  growth  are  al 
al).sent.  Iiiit  whenever  this  forms,  it  ^mows  less.iliundantly.  c;irriei 
many  eno(,r}ie<l  Mood-ch.iiUK'ls  and  tul.ules  with  old  hlood-pi^'- 
inent.    .md   throuiihout    has  a   char.iclerislic,  p.-de.  .edematous 
apiM'arance,  with  considcral.le  Hhrillar  stretchin-r.     S«'hmausand 
Ihtrn  "'  have  |>oiiited  out  th.-it  all  ves,s(.|s,  .arteries.  :itid  veins  are 
here  enormously  thickene<l. 

The  considenition  of  the  secondary  contracted  kidney  has 
already  ushere.l  in  certain  new  prol.leins,  which  I  have  either 
only  t«mche(l  u|M)n.  or  held  over  for  the  con.siderjition  of  the 
productive  ty|M>s  (,f  nephritis,  to  which  we  will  next  devote  our 
attention. 


.so 

s 


FIITM   IJKTrHi:* 

l'Uo|)t(TIVK        NkI'IIHITIS.      (HWCiKS        |\       OtIIKI 


ViSIKHA. 


(Ki 


)K.MA 


(i<  nllinicii: 

I  turn  t«)-<|jiy  t<»  the  last  cliMplcr  of  nephritis,  to  the  considora- 
tion  of  that  ty|M'  I  j:roii|M'<l  as  proihutivi'  nephritis,  and  which 
is  usually  spoken  of  as  chronic  interstitial  nephritis.  I  helievp 
that  its  apiK'arance,  at  least  j;ro.ssly.  is  familiar  to  you.  We 
understand  liy  it  an  e.xtn'rne  atrophy  of  the  pan-nchynia,  with  ati 
abundant  increase  in  fihrous  ti.s.sue.  Such  a  kidney  is  ver>- 
.small:  the  smallest  kidneys  on  record  arv  of  that  tyjK'.  The 
surface  is  extremely  irre«rular  in  the  uncomplicated  |)ure  cases, 
liiiely  jrramilar.  with  delicate  cicatricial  c«)ntractions.  It  is 
cither  reddish  in  color  or  pale,  sometimes  yellowish  pale.  On 
section  it  is  jM'rfectly  evident  that  there  is  a  marked  diminution 
and  loss  of  kidney  substance,  particularly  in  the  cortex  most  of 
it  may  have  completely  disap|H'ared.  In  ca.ses  complicated  with 
arterio-sclerotic  infarctions  deep  cicatrices  form  and  interchanjje 
with  the  finer  v:ranulations.  The  normal  markinjjs  are  U-sually 
cntin'ly  ol)literated.  (Jlomeruli  and  jilomerular  rows  cannot 
often  Ik'  made  out  at  all.  The  jtlomeruli  apjM'ar  mort>  frequently 
on  the  cut  surface,  in  the  form  of  small.  |K)int-like.  pale  hyaline 
elevations.  On  the  other  hand,  in  places,  umisually  dilated, 
irrcfiuhir  v.-iscular  channels  run  through  the  cortex.  That,  a.s 
.\(iu  will  appreciate  in  a  monient,  is  pnnluce*!  I»y  the  j)eculiar 
<ir(ulatory  modifications  which  prevail  in  this  kidney.  The 
intervening   tubular   parenchym.-i.   de|H'ndinji   on    the   va.scular 

•  Di'liviTccI  nil  I'l-lirimry  22.  VMKK 
13  IHI 


ItlJ 


KKKillTs    IHsKASK 


••oiidilinii.  is  citlHT  (piii<>  pale  or  pinkish.  Siii.illcr  aiitl  larger 
cysts,  sniiiciiiiifs  ;u(|iiiniiy  coiisitlcralilc  iliiiicrisiitiis,  nrv  also 
conmioiily  ilistriluUrtl  throiiirli  (lie  corlcx.  (MTasionally  at  the 
junction  of  nicilulla  and  cortrx,  ran'ly  (l('«'|H'r  in  the  pyianiids. 
As  a  rule,  lliis  linr  of  dcinaication  U'twccn  cortrx  and  incdiilla 
is  poorly  defined,  except  in  cases  wlien-  stasis  li.as  complicated, 
wlien  the  vess«'|s  of  the  pyramids  are  nniisnally  prominent, 
:ind  nuliale  well  into  the  cortical  remn.ants.  Sometimes  cilcium 
or  urate  de|Misits  m.iv  lu're  \h>  s(>en.  When  inflammatory  exacer- 
li.ili«>ns  li;iv«"  su|»ervened.  or  hastened  the  final  termination,  ihe 
whole  kidney  a|)|K"ars  more  difTnsely  rddened  or  mottled.  In 
c;:ses  of  f.ir  .advanced  contraction  the  pelvis  is  rel;itiv«'ly  very 
l.irnc  and  very  fatly.  The  fat  extends  well  upward  U'tween 
the  atrojihied  pyriimids.  \ery  prominent  .are  the  thickened 
arteries.  This  thickenin<:  may  involve  only  the  smaller  ones, 
which,  on  section.  stan<l  out  prominent  and  ^i.apin^.  or  it  may  j-o 
so  far  as  to  .dTecl  the  renal  .irtery  iFiy:.  \',ii. 

Two  (piestions  pres<'nt  themselves  to  us  from  the  start: 
Wh.it  is  the  rel.ition  of  this  form  of  nephritis  to  the  chan>res 
previously  discu.s.s«>d,  particailarly  tlie  s<»-calle«l  .s<.con<lary  con- 
tracted kidney?  .and,  s<'condly,  \\h,it  is  the  relation  of  th.it  ex- 
treme parenchym.itous  Ictss  to  the  ahimdaiit  filirous  ti.ssue  pro- 
liferation? 

\\  ith  regard  to  the  first  cpiestion.  you  recall  that  Hri^rht.  who 
took  a  uniform  view  of  the  whole  nephritic  process,  n^arded  the 
conlr.acled  kidney  .is  the  last  slajie  of  the  previous  two.  and  a 
siniil.ir  view  w.is  entertained  liy  many  siil>s«'(|U«'nl  in\esti;:ators. 
nolal»l.\     iienle.    Heinhardl.    i'rerichs.    and   especially    Wei;ierl. 

'•ii  tl llici"  hand.  Christ ison.  while  acknowl«'dy:in;i  this  to  some 

extent,  was  the  first  to  doiilit  th.at  .dl  these  v.arioiis  lesions  were 
st.iv:es  of  one  inorliid  process.  This  ir.-iined  much  support  in 
Kiiyland  in  the  works  of  .Johnson.   TovnlMe.  Simon,  and  Husk. 


Hk  1-|.  Ncpliniis  iir.i<Iiii-(iva.  Kidnoy  uniall.  woiplit  .V.Rnis,  fnmi  a  woman  f(.rtv- 
-is  yarv  i.M  Siirfai-.-  flail,  iicl  ami  fiii<  ly  Knimilnr,  pal.-.  (  i.rt.x  iiiillc.nnlv  an. I  nurk- 
.  illy  iiarnmvil,  si.  lliat  II,.-  I.li.r  |.ns.TV((l  niiijiijla  a|.|Karv  .Irawii  U.  llic  MirtaV.-  .\,,rinal 
iiiaikiin;-  l.'^t  Wliitisli  ar.a>  .maliir.'  filin.iis  tisKii...  intcriiiunjrc  will,  r.il.li>l,  va^.iijar 
L-i:nHiIan..n  li-Mi.)  ..r  y.jl.m  i-l,  i.,l  |K-,rli<.  All  vi>,s<N  .li.-tinctiv  il,lrk.n.-.l.  ar..iin.l  ili.ni 
iiv.|ii.iiily  »liii.'  Iil.rouii  iMitclies.  I'elviB  iflulively  lam-.  lUn-  uIm»  wac  u  t.miinal 
iil.riiionji  iiencunlitia. 


I 


MtCROCOTY    RfSOlUTION    TEST    CHART 

ANSI  ond  ISO  TEST  CHART  No    2 


1.0 


I.I 


lU;  I  2.8 


1.4 


m 

2.2 


1.8 


1.6 


.^  -'APPLIED  IN/MGEJn 

^P.  '6'._1    tasi    Mji-^    ilr-e! 

y.^  «oc''ester,    N«<k    ririrt,  T4609        USA 

^—  L^'fe)    *8;  -  CJOO  -  Phon» 

^B  (7t6)   2M  -  59B9  -  Fo> 


I'KODlCTn  K  XKI'HHITIS.       VISCKKAI.  (  MANCiKS.       (KI)KMA      KV.i 


with  which  wo  iK'came  fainihar  in  the  first  lecture,  until  finally 
Sanniel  Wilks  and  (Irainjrer  Stewart  re<iar(le(l  the  lar<:e  white  and 
the  small  <iranular  kidneys  as  independent  affections,  and  (iuU 
and    Sutton  even    s{)oke  of   "  arteriocapillaiy   fibrosis"  as  the 
cause  of  contracted  kidney.     Similar,  althouiih  not  so  radical, 
were  the  ideas  of  Hart  els  in  (iermany,  who  definitely  separated 
the  so-called  primary  interstitial  nephritis  from  the  others;    in 
this  he  was  followed  by  Ziejiler  and  his  pupils.     Senator,  you 
remember,  took  a  somewhat  reconcilinji  view,  inasmuch  as  he 
holds  that  all  these  various  forms  may  l)e  definitely  related,  or, 
on  the  other  liand,  may  develop  independently,  and  also  result  as 
the   consequence  of   primary   arterial   chanjies.     Inflammatory 
e.xacerbation  in  them  may  occur  at  all  times.     Finally,  the  ten- 
dency on  the  part  of  some  modern  patholoj^ists  and  clinicians 
^hlrchand,  Loiilein,  Miiller     seems  to  be  ajiain  toward  the  older 
uniform  view  of  Brijiht.     It  has  In^en  pointed  out  by  them  that 
it  is  extremely  difticult,  if  possible  at  all,  to  separate  the  sec- 
ondary contracted  kidney  from  the  so-called  primarA-  interstitial 
nephritis,  and  that,  in  all  probal)ility,  many  of  the  latter  are  the 
results  of  previous  exudative  inflammatory  conditions,  which 
have  remained  latent  or  projjressed  exceedinjily  slowly.     It  has 
been  claimetl  by  some  that  the  secondarA-  contracted  kidney  is  an 
aniemic  one,  in  which,  even  after  much  loss  of  sub.stance,  the 
dejienerative  features  still  predominate,  and  that,  on  the  other 
hand,  the  primary  productive  nephritis  api)ears  as  the  typical 
small  red  kidney.'     A<iain.st  this,  however,  it  has  been  urjied 
that  the  small  red  contracted  kidney  represents  only  a  later  stajie 
of  the  lar^e  hemorrhajiic  de<ienerative  nephritis,-'  which  has  a 
much  fireater  tendency  to  contract,  on  account  of  better  imtri- 
tion  and,  therefore,  leads  to  al)undant  connective-tissue  forma- 
tion.   My  own  exjH>rience  in  the  matter  has  led  me  to  believe  that 
there  is  no  essential  anatomical  difference  in  anv  of  the  chansres 


-•a 
■'I  I 


I 


H)4 


UUKiHT  S    DISKASK 


which  (tccur  in  this  ty[U'  of  product ivc  nephritis  from  those  which 
we  observed  in  the  other  forms  and  which  we  have  discussed  in 
detail.  On  the  other  hand,  it  cannot  l)e  denied  that  there  exists 
a  nephritis  the  developm<>nt  of  which  differs  in  certain  points 
from  those  we  have  considered:  Inflammator>-  features  are 
neither  so  intense  nor  so  fjeneral  and  diffusely  distributed  from 
the  start  as  in  the  ty|)es  of  nephritis  previously  discussed.  The 
process  pre.sents  itself  as  a  jiradually  advancinji,  patchy  inflam- 
mation, leadinfi  to  a  proj^re.ssive  loss  of  circumscribed  area>s 
of  kidney  substance,  while  other  parts  are  preserved  and 
their  functions  continued  and  c(mi{)ensated.  (Iradually,  by 
chanjred  anatomical  conditions,  an  unusually  complicated  orjjan 
is  thus  formed,  whose  functions  show  marked  abnormali- 
ties. On  account  of  this  slow  projrress  and  a  fjradual  adapta- 
tion of  the  or«ranisni  to  the.se  conditions,  it  is  compatible  with  a 
lonjrer  jM'riod  of  life.  Such  a  kidney,  however,  is  easily  vulner- 
able, and  may  experience  at  any  time  an  active  and  diffuse  in- 
flammatory exacerbation,  placinji  it  in  the  catefj;or\-  of  the  types 
previously  studied. 

I  am.  therefore,  of  the  opinion  that  anatomically  no  particular 
feature  differentiates  any  of  the  contracted  kidneys  one  from  the 
other,  but  ix'lieve  that  the  mode  of  orijrin  and  development  may 
differ.  It  may  result,  first,  from  a  diffvi.se  inflannnation  (the 
so-called  secondary  contracted  kidney),  or,  .secondly,  very 
insidiously.  ;is  the  con.secjuence  of  .slowly  pro<!;ressive  circum- 
scribed inflammatory  foci,  which  elinunate  kidney  substance  ver>' 
slowly,  and,  therefore,  normal  functionatin<r  parenchyma  is  re- 
tained for  a  considerable  time.  This  distinction  is  in  reality  a 
purely  relative  one.  and.  taken  with  the  time,  accounts  for  certain 
modifications  in  one  more  fretiuently  than  in  the  other.  In 
the  end  the  result  is  the  same,  luit  may  be  considerably  hastened 
bv    infiammatorv    exacerbations.     From    this    stand|K)int    an 


ii 


I'KoniCTIVK  NKIMIKITIS.       VISCKKAL  CH AN(iKS.      (KDKMA 


!().-) 


essential  differenee  l)etwpen  primary  and  seeondary  contracted 
kidneys  does  not  exist,  except  in  the  localization  and  projiress 
of  the  (lise:is<\  and  both  are  really  secondary-  to  previous  dejiener- 
ation  and  exudation,  in  one  with  a  latent,  in  the  other  with  an 
active,  course. 

The  terms  primary  and  secondary,  contracted  and  interstitial 
nephritis  are  misleadinji,  ther(>fore,  and  had  l)etter  l)e  drop{x>d 
altojrether.  Anatomically,  we  should  speak  of  productive 
nephritis,  then,  when  the  exudative  and  dejienerative  attributes 
are  less  prominent  and,  on  the  other  hand,  the  formation  of 
connective  tissue  ver>-  abundant.  It  is  evident,  therefore,  that 
the  causes  of  productive  nephritis  are  ver>'  numerous.  It  may 
either  result  from  a  previous  diffuse  exudative  degenerative 
nephritis  which  has  underj^one  remission  and  cleared  in  certain 
areas,  so  that  conditions  for  a  patchy  projjress  of  the  disease  are 
thus  created;  or  it  develops  ver\-  insidiously,  usually  quite 
unknown  to  the  individual,  until  it  reaches  an  advanced  degree, 
and.  as  the  consequence  of  lonjr-continued  intoxications— lead- 
poisoning,  etc.,  gout,  and  probably  metabolic  autointoxications. 
These  may  lead  directly  to  patchy,  irregular  injurj-  and  corre- 
sponding inflammator\'  foci,  with  eventual  loss  of  kidney  sub- 
stance. 

In  the  description  of  this  productive  nephritis  we  may  safely 
disregard  all  the  various  changes  which  presented  themselves  to 
us  before,  and  devote  our  tittention  mainly  to  those  characteristic 
features  which  appear  especially  accentuated  in  it. 

From  these  considerations  it  Ix'comes  intelligible  that  the 
kidney  of  a  productive  nephritis  offers  the  greatest  variety  of 
pictures.  It  represents  really  a  combination  of  all  the  inflamma- 
tory- features  which  we  previously  discussed.  P'ar-advanced 
fibrous  areas  with  hyaline,  contracted  glomeruli,  lost  or  dis- 
torted tubules,  may  change  abruptly  to  Ix-tter  preserved  and 


ill  2 


i(;() 


HKHillT  s    DISKASK 


t    i 


even  licnltliy  kidney  parenchyma  in  tlie  state  of  conipensatory 
iiyjM'rtropliy.  I'liis.  ajiain,  adjoins  patches  of  kidney  substance 
which  are  the  seat  of  recent  intiaininatory  dejienerative  and  exu- 
dative foci.  The  latter  are  particularly  prominent  in  the  intor- 
tuhular  tissue,  and  consist  of  lym))hocytic  and  polyhlastic  cells, 
which,  accompanied  hy  fihrohlastic  proliferation,  soon  lead  to 
considerai)le  stretchin.ir  and  thickeniii}:  of  the  intertuhular  tissue, 
and  the  formation  of  waxy,  mature,  fibrous  conjiective  tissue. 
Similar  lesions  prevail  around  and  within  the  jjlomeruli,  and  as 
we  h.ive  become  fully  a(<iuainied  with  them.  I  shall  not  discu.ss 
them  here  anain.  On  account  of  the  slow  and  patchy  projiiess 
in  these  chaniics,  an<l  the  compensatory  possibilities,  the  mitri- 
tioM  of  the  orjiati  is,  as  a  rule,  in  much  l)ett(>r  state  than  in  the 
cases  of  brusipie  and  jiCMieral  ii(>phritis.  where  inflanunatorv  de- 
tritus and  iiener.'il  inflanunatory  swellini:  seriously  i)lock  the  mi- 
tritive  charuiels.  As  a  conse(|uence  the  production  of  new  cells 
;.nd  til)rous  tissue  occurs  here  with  nuich  ureater  abundance 
;.nd  [)erfection  than  would  be  possible  under  these  conditions. 

These  ^  ery  slow  developnuMits  are  also  responsible  for  a 
complete  and  permanent  new  arranucment  of  the  components 
of  the  kidney.  I  consider  this  of  the  sireatest  imi)ortance.  as  it 
.iccounts  in  no  small  decree  for  some  of  the  perplexing  functional 
(h'viations  which  ar(>  very  characteristic  and  constant.  These 
anatomical  chanji<'s  manifest  themselves  in  the  paren<'hyma  and 
in  the  vascularity  of  the  kidney.     Hoth  are  intimately  comiected. 

In  the  tubules  two  chanjies  occur:  First,  a  ccmiplete  rejienera- 
tion  f)f  epithelium,  of  the  type  which  we  met  before  low,  smooth 
and  .syncytial,  endothelial-like.  On  the  other  hand,  it  is  not 
unconmion  to  ob.serve  the  formation  of  hiiih,  cylindrical  epithe- 
lium within  old  tubiiles.  One  or  the  other  chancre  is  so  jieneral 
that  we  may  .safely  .say  that  the  kidney  <rradually  accpiires  an 
entirely  foreii^n  epithelium,  beinji  inorpholo;;ically  and  undoui)t- 


I'UODICTIVK  NKI'HHITIS.       VISCKHA!.  CHANCKS.      CKDKMA      167 

cdly  functionally  (listiiict.  and  diffprent  from  its  prodecossor.  It 
is  most  conspicuous  in  tho  convoluted  tubules.  Secondly,  the 
tuluiles  chan«:('  their  size,  shajK",  :ind  c<)urs<'.  They  l)econie 
more  tortuous,  ;ire  fre(|uently  of  an  adenomatous  type,  ii\\'u\ii 
rise,  therefore,  to  a  ditTerent  jrlandular  system  from  the  normal 
uriniferous  tul)ule. 

Of  greatest  importance  is  the  elimination  of  the  filonjeruli,  as 
it  necessitates  and  accomplishes  an  entire  change  in  the  circula- 
tion of  the  kidney.  It  has  been  shown  by  Thoma  '  that,  where 
irlomeruli  become  impenneal)le.  circulation  may  l)e  kept  up  l»y  a 
direct  union  of  afferent  and  efferent  vessels,  so  that  l)loo<l  reaches 
the  tubules  direct,  without  circulation  throujih  the  glomerulus. 
On  the  oth(>r  h.-md,  in  places  wlH>re  complete  loss  of  cortical 
substance  has  taken  place,  compensatory  dilated  channels  form 
in  the  cortex:  finally,  when  this  becomes  impossible  by  destruc- 
tion of  whole  cortical  capillary  systems,  medullary  vessels  are 
pressed  into  service.  Under  such  conditions,  the  blood  reaches 
the  medulla  directly,  avoiding  the  cortex  altoficther.  This  is 
lirossly  well  illustrate<l  by  the  appearance  of  abnormal  and  enor- 
mously dilated  vascular  channels  within  the  cortex  and  medulla. 

You  are  now  in  a  position  to  appreciate  that  in  the  well- 
develoiK'd  ca.ses  of  this  type  of  nephritis  we  are  dealinj:  with 
kidneys  which  represent  entirely  reconstructed  or<ians.  The 
glomeruli  have  been  eliminated,  the  tubules  have  not  only 
chanjjed  their  epithelium,  but  also  their  cour.se,  and  the  whole 
vascularity  of  the  or<>an  has  been  altered.  No  blood  circulates 
tliroujih  filomeruli.  and  nuich  avoids  the  cortex  altoj^ether.  to 
proceed  directly  to  the  medulla.  .\s  the  consetpience  of  these 
essential  interferences  with  the  structure  of  the  kidney,  far- 
reachinji  fvmctional  modifications  nece.ssarily  develop,  va.stly 
different  from  anythin<r  ever  observed  imder  physiolo<>ical  con- 
ditions.    You   readily   understand  how  difficult    it   will   be  to 


d 


II 

I  I 
:  f 


H 


I(»S 


MKKillT  S    DISKASK 


explain  the  functions  of  such  a  radically  clianjicd  or>ran  on  the 
hand  of  siniph'  physiolo^iical  experience. 

Hut  iM'fore  sketchinji  these  patholojiical  functions  for  you.  we 
must  '-onsidersonieothj'rniorpholojiical  features  of  this  nephritis. 

Of  v.rf':it  fre(|uency  are  cysts.  'Ihese  occur,  sometimes  few. 
at  other  times  in  jireat  tunnher,  so  that  tlie  name  (»f  actpiired 
cy.stic  kidney  has  been  <iiven  to  such  cases.  The  size  of  the 
cysts  also  varies  <:reatly.  From  small,  point-like  prominences, 
they  may  <rrow  to  jrrape-sized,  or  even  e<r«-sized,  jrlohular  bodies, 
but  never  to  the  dimensions  of  the  con<:enital  cysts.  The  larjier 
ones  contain  usually  a  thin,  watery,  clear  fluid;  in  the  .smaller 
ones  inspissated,  yellowish  or  ■rreeni.sh  material  is  not  infre- 
(juently  found.  These  latter  may.  as  Havun^  has  .shown,  calcify. 
The  orijrin  of  these  cysts  is  twofold.  In  the  first  place,  they 
repres(>nt  parts  of  isolated  uriniferous  tubules,  which,  havin^^ 
been  cut  off  l)y  the  sclerosing;  inflanmiati(m,  underjjo  cystic  dila- 
tation. It  is,  therefore,  held  by  some  that  the  cyst  fluid  repre- 
sents retained  urine.  But  the  different  nature  of  the  lining 
epithelium  of  such  cysts,  as  well  as  the  phy.sical  and  chemical 
character  of  the  fluid,  makes  a  modified  .ecretion  probable.  On 
the  other  hand.  I  observed  a  jjood  many  years  ajio  in  1895, 
while  workinj!;  in  VViirzhurfi  that  some  of  these  cysts  are  dis- 
tinctly of  jilomerular  orij-in.  This  can  l)e  directly  oiwerved  in 
certain  smaller  ones,  where  location,  size,  and  arrangement  of  the 
wall  and  linin<r  epithelium  stamp  the  cyst  Ixxly  as  of  jjlomeruhir 
derivation.  Such  cystic  bodies  frecjuently  contain  what  I 
considered  remnants  of  the  jilomerular  tuft.  I  held  the  opinion 
that  these  cysts  owed  their  ori<:in  either  to  a  sclero.sinji  inflamma- 
tion or  to  a  stajrnation  in  the  upper  parts  of  the  tubules.  Haum. 
however,  who  has  investigated  that  mattj'r  later,  regards  them 
as  conjjenital.  and  as  an  incompletely  develo{M'd  filomerulus. 
Hut  his  arjitmients  are  not  entirely  conviiicin;:. 


I'UODICTIVK  NKl'HKITIS.       VISCKHAI.  CHANCKS.      <Kf)KMA      l()i) 


Of  the  jsroatpst  iniportiiiici'  nnd  intoivst  aro  the  vascular 
cliaiifics.  'I'ho  arterial  chaiijics  in  nr|)liritis,  like  thos*'  occurrinji 
(uitsidc  of  it,  have  Imtu  ii  much-discussed  subject,  and  even  now 
there  is  no  exact  ajrreenient  as  to  tlieir  pathofienesis  and  relation 
to  the  nephritic  process.  We  may.  I  iK'Ueve,  differentiate  here 
iK'tween  two  t\}K's  of  arterial  thickeninji  which  de|MMHl  partly 
upon  the  local  inflammatorv-  chanjies  and  partly  upon  the  results 
which  outside  influences  pnxhue  in  the  arterial  system  of  the 
kidney.  Consecjuently  we  may  dilTerentiate  l)etween,  first,  an 
inflammatory  thickening  (le|H'ndent  upon  tlv  local  lon<:-con- 
tinued  productive  inflammatorA'  processes.  'Ihis  plays  a  part 
primarily  in  the  adventitia  of  the  vessels.  Ferivasciilar  infiltra- 
tions comhifie  with  fihroMa.stic  proliferations  and  lead  to  thick- 
eiiiiifi  of  the  adventitia.  Fretiuently,  however,  the  lesion  pro- 
<:re.sses  toward  the  lumen  of  the  ves.sel,  thereby  addinjj  an 
endarteritis  fil)rosa  oi)literan.s.  The  latter  is  particularly  the 
ca.se  in  the  .smaller  vessels,  and  may  possibly  al.so  l)e  traced  to 
a  direct  toxic  action  on  the  intima. 

Second,  the  vessels  may  show  a  process  of  arteriosclerosis  or 
atherosclerosis.  The  relationship  of  this  to  nephritis,  partic\i- 
larly,  has  been  a  much-discussed  matter. 

We  owe  primarily  to  .lores,*  and  later  to  him  with  Pr\m,'  an 
extensive  study,  not  only  into  the  histolofiy  of  the  lesion,  but 
also  into  the  gradual  development  of  the  arteriosclerotic  process, 
and  lately  Fahr"*  has  added  a  study  with  particular  reference  to 
the  kidney.  .lores  and  this  has  been  corroborated  by  others 
distinjiuishes  between  two  ty|X's  of  arteriosclerosis:  First,  hy- 
jK'rplasia  of  thick  elastic  lamelhr,  which  are  derived  from  the 
internal  elastic  membrane.  This  is,  in  reality,  a  perfectly  phy- 
sioloftical  {)rocess  which  may  be  traced  from  early  childhood. 
This  thick,  elastic,  internal  membrane  displays  a  jjreat  tendency 
to  dejteneration  and  fibrillar  disintefiration,  associated  with  fatty 


N 


17(1 


UKKillTS    hISKASK 


(Icjiciicratioii  itf  tlic  piirt.  .lores  r(';i;ir(ls  llicsc  pniccsscs  as  the 
•  •ssciitial  feature  of  the  arterictsclerotic  pnteess.  'I'his  in  turn  is 
followed  liy  connect ive-t issue  formation.  S'condly,  .lores  de- 
scrilies.  as  a  distinct  process,  a  simple  coimei-t  ive-t  issue  prolifera- 
tion of  the  intini.'i,  the  so-called  endarteritis  fihrosa.  He  looks 
upon  the  juratlual  f«trm.ition  of  the  elastic  lameihe  as  a  com|X'n- 
satorv  process,  one  that  is  necessary  for  th<'  m:dntenance  of 
arterial  elasticity.  These  views  are  oppo.sed  to  those  oriiiinally 
offered  hy  'i'lioma.'  and  als(»  ilwald'"  and  Friedeman."  Hind- 
lleisch,  and  olhers,  who  look  upon  the  rise  in  hlood-pressure  as  a 
cause  of  arteriosclerosis. 

Corrolioration  and  extension  of  .lores'  views  have  recently 
l)een  advanced  hy  ["ahr.  lie  not  only  traced  the  same  develop- 
ment of  the  process  from  early  childhood  to  old  ajic,  l)Ut  drew  at- 
tention to  the  fact  that  in  the  heart  appears  early  a  fine  elastic 
network,  which  durinti  later  life  may  take  on  considcrahle  dimen- 
sions. I'ahr  hrinus  this  into  analojiy  with  the  arteriosclerotic 
|)rocess.  On  the  other  haiiil.  he.  and  al.so  Hoth,'-'  emphasize  the 
fact  that  the  occurrence  of  arteriosclerosis  it)  the  kidney  seems 
to  JK'ar  no  relation  to  the  nephritic  |)rocess.  This  is  particularly 
corrohorated  in  the  nephrites  of  the  youiifr.  when,  in  spite  of  hijih 
idood-pressure.  little  or  no  hyperplasia  of  the  intima  occiu's. 
Ajrain,  this  may  he  marked  in  cases  when  no  productive  ne|)hritis 
can  he  demonstrated. 

Based  on  his  ol)servations.  Fahr  concludes  that  arterioscle- 
rosis of  the  renal  arteries  is  an  extremely  frecjuent  phenomenon. 
It  may  assume  considerable  dimensions  without  seriously  inter- 
ferinji  with  the  kidney  .structure.  On  the  other  hand,  it  mjiy 
lead  to  conditions  which  in  time  produce  extensive  contractions 
of  the  or<ran.  The  ojiposite,  h()wev(>r,  arteriosclerosis  as 
results  of  a  nephritis  plays  only  a  very  subordinate  role. 
I"'ahr  l)elieves,  therefore,  with  Marchand,  that  the  arteriosclero.sis 


I'HuniCTlN  K  NKPHHITIS.       VISCKHAI.  <H.\N<iKS.       (KDKMA     171 


i ,   .  f-  -,1 


rill    U    -Maiki-il  vascular  tliickcniiin  anil  iiarniwiiiu  in  senile  and  arteriosclerotic  kjilr.cy. 

X  IIJ, 


f; 


ill 


ill 


PHonrCTlVK    NKI'HKITIS.     VIWKKAI.   CHAXOKK.     (KDKMA      IT.i 

of  rnial  \ts»«'1s  is  not  thr  result  of  a  nephritis  nor  of  rai.s<'«l 
}:eneral  liUMxl-pn'ssure,  but  the  expn>ssion  of  the  <h»ily  variations 
ill  l)|(M)(l-pn'ssun'  in  a  xascular  or^an,  to  which  ever>-  indiviciuiil 
is  jnon>  or  less  ex|X)se(i.  (Ie|)eii(linn  u|M»n  occiipation,  tein|H'ra- 
inent,  and  mode  of  living.  In  other  words,  a  wear  and  tear 
process. 

I  iM'lieve.  however,  that  it  cannot   Ih'  denied  that  lonp-eon- 
tinued  increa.sed  n>sistaiice  in  the  kichiey  as  the  ivsult  of  ob- 
literation of  normal  vascuhir  paths  may  l)e  a  factor  in  producing 
ehistic  thirkeniiifi  of  renal  vessels.     This  view  was  particularly 
advocated  by  llindfleisch.     A  combination  may.  therefore,  occur 
with  the  third  vascular  chanpe,  which  may  l)e  observed  in  these 
kidneys,  which  con.sists  in  a  hy|)ertrophy  of  all  the  coats,  partic- 
ularly (»f   the   nudta.     This  has  Ix'en  emphasized   by   Friede- 
nuin.'*  who  separated  this  lesion  distinctly  from  the  arterio- 
sclerotic process,  although,  as  you  ai)preciate,  it  may  lead  to  or 
combine  with  it,  so  that  a  shaq)  line  of  distinction  cannot  always 
l)e  drawn.     This  process  is  characterized  mainly  by  a  hyper- 
plasia of  the  nui8cle-fil)ers  of  the  media,  which  distinjjuishes  it 
from  ftranulomatous  arteritis,  endarteritis,  and  arteriosclerosis. 
In  them,  you  rememl)er.  there  occurs  essential  lo.ss  of  muscle 
tissue,  with  fibrous  or  elastic  tissue  n>placement .     Indeed,  Adami 
looks  uix)n  this  as  the  es.s<Mitial  feature  of  arteriosclerosis.     The 
arterial  muscular  hy|)ertrophy.  however,  has  l)een  traced  to  the 
same  causes  which  demand  excessive  muscular  contraction  el.se- 
where,  and  which,  as  we  will  see  later,  find  marked  expression  in 
the  hypertrophy  of  the  heart .     But  here  ajrain  the  local  conditions 
and  firatlual  increasing  imp<>rmeability  of  the  vascular  paths  in 
the  pwfiress  of  a  nepnritis  may  also  play  a  role. 

Finally,  the  capillaries  show  inflammator>-  endothelial  pro- 
liferation. This  neces-sjirily  leatls  to  thickeninji  of  their  walls, 
and  frequently  they  under^jo  hyaline  transformation. 


Hi 


174 


HliKJHT  S    DISKASK 


\\v  SCO.  therefore,  th.-it  the  thickeiiiiifi-  of  the  vessels  whieh  is 
observed  (hiriiii;  the  pro^jress  of  ;i  iiejjhritis  orijriiiates  either  from 
coiKUtioiis  arisiiiii  within  or  outside  of  the  ki(hiey,  and  that,  as 
in  tiie  hypertrophy  of  tlie  elastic  tissue  and  the  media,  hoth 
factors  ma\-  lie  active.  Hut  whatever  may  lie  their  orijiin.  they, 
in  turn,  are  ;ipt  to  very  materially  influence  the  proj-ress  of  the 
lesion.  'I'his  occurs  particularly  in  the  arteriosclerotic  and 
the  inflammatory  end.-irterial  chanjics.  'I'hese  are  naturally  fol- 
lowed l)y  marked  diminution  in  the  caliher  of  the  ve.s.sel,  and.  in 
time,  lead  to  thrombosis  ;ind  complete  obliteration  of  the  thus 
affected  va.scular  channel  (Fiji.  44 1.  '{"lie  n'sult  of  such  an 
occlusion,  however,  has,  particularly  in  larjier  vessels,  a  decidedly 
l>ad  elTect,  as  it  is  necessarily  followed  by  infarction  of  the  area 
supplied  by  that  vessel.  That  part  underji(!(%s,  therefore,  ne- 
crosis, is  entirely  lost,  and  heals  only  with  the  formation  of  a 
deep,  thick  scar  ( i'ii;.  42i.  .\linost  all  advanced  cases  of  pro- 
ductive nephritis  show  these  evidences  of  previous  infarctions. 

This  leads  directly  to  the  consideration  of  the  so-called  ar- 
teriosclerotic and  s(>nil<>  kidney,  which  is  usually  cla.ssified  as  the 
arteriosclerotic  type  of  productive  nephritis.  I  speak  of  it  as 
sclerosis  or  atrophia  renum,  iK'cau.se  its  inflanmiatory  nature 
appears  very  doubtful.  It  is  the  typical  senile  kidney,  and  on 
account  of  some  .similarity  to  the  productive  types  of  nephritis, 
has  fre(|uently  Ixen  considered  as  identical  with  it.  There  are. 
nevertheless,  certain  features  which  justify  its  separation  from 
the  inflannnatory  productive  nephrites. 

As  the  nam(>  implies,  this  kidney  appears  durinji  later  life. 
.\o  definite  i  ime  for  its  development  and  occurrence  c.-mi  be  miven, 
;iny  more  th;in  an  exact  answer  to  the  (luestion.  When  do  people 
aiic?  Indeed,  the  senile  kidney  is  dependent  upon  the  jieneral 
process  of  ajiinjiof  the  whole  individual,  and  more  particularly 
upon  the  conditions  of  its  circulatory  ap[)aratus.     It  is,  therefore, 


il 


Kit:.  I">.-  Atnipliiii  senilis  arloriosclorotica.  Wripht  5()  Kms.  F'roni  a  woman,  stncnty- 
four  years  old,  who  died  of  friiiijrreiie  of  )jiit  due  to  arterioselerot  ie  thrombosis  of  arteria 
meseraiea  su|)orior.  Kxtreme  loss  of  whole  kidney  sulistanee.  and  thickeninR  of  renal 
arterj-.  Idiopathic  hydronephrosis  extending  to  cystic  dilatation  of  the  medullary 
pyramids. 


II 


'Koni  I'TIVK  NKI'MHITIS.       \  ISCKKAI.  (•HA\(;KS.      (KDKMA      175 


eminently  a  nutritive  (li.sturl)an('e,  into  the  prfxiuction  of  which 
three  factors  enter:  First,  and  paramount,  the  condition  of  the 
blood-vessels  of  the  kidney;  second,  the  condition  of  the  jieneral 
circulation;  third,  certain  orjtanic  cellular  chanfjes  incident  to 
advanced  life. 

In  our  previous  discussion  about  the  arterial  changes  we 
learned  that  the  vessels  of  the  kidney  are  particularly  exposed  in 
an  unusual  de^'ree  to  the  wear  and  tear  of  life.  Outside  of  the 
spleen,  there  is  perhaps  no  other  orjian  which  is  so  constantly 
imder  marked  variations  of  pressure,  tension,  and  rapidity  of 
blood-current.  All  the  arteries  in  advanced  life  show  evidences 
of  strain  in  the  form  of  the  various  processes  collectively  jrrouped 
under  the  term  of  arteriosclerosis  or  atherosclerosis,  but  for 
reasons  just  mentioned  it  reaches  in  the  kidney  more  jjeneral  and 
much  ftreater  dimensions.  With  Fahr  and  Marchand  we  may 
look  upon  renal  arteriosclerosis  as  physiolojjical  for  advanced 
life;  so  it  hapi)ens  that  a  characteristic,  rather  constant  feature 
of  the  senile  kidney,  recojjnizable  almost  at  first  sijiht,  is  pro- 
nounced thickennijr  and  narrowinj:  of  its  vessels. 

The  results  of  these,  and  {K)ssibly  still  other,  interferences  with 
the  nutrition  of  the  parts  show  themselves  in  parenchymatous 
atrophy  of  circumscril)ed  areas  of  the  kidney  substance.  The  glo- 
meruli and  the  connected  tubules  shrink,  become  hyaline,  and 
thus  the  involved  portion  collapses.  This  loss  of  substance  gives 
rise  to  the  formation  of  slowly  maturing  granulation  tissue,  rich 
in  engorged  blood-vessels,  usually  taking  origin  around  vessels; 
comiMMisatory  and  sometimes  consideral)le  enlargement  of  the 
neighboring  structures  follows,  unless  they  also  have  become  in- 
volved in  a  similar  fat(>.  The  process,  which  commences  in  small 
patches,  may  finally  affect  a  considerable  portion  of  the  whole 
kidney  substance.  Henmants  of  tubules  have  Ix^come  buried 
within  the  increased  fibrous  tissue  as  adenomatous  loo[)s  or  as 


f:% 


I7(i 


HHKiHT  S    DISKASK 


cystic  papillary  IxmHcs.  Small  hyaline  "ilohulps  may  Ih'  the  only 
evidences  of  previous  jilomenili.  The  kidney,  as  a  whole,  dimin- 
ishes therefore  in  size  and  ap|K>ars  irre<;ularly  jiraimlar,  and,  de- 
{)endinji  upon  its  vascularity  and  the  presence  or  al)sen('e  of 
serous  inil)il)ition.  which  I  will  discuss  in  a  moment,  is  either  red 
or  pale. 

This  state  of  affairs  has  almost  always  added  to  it  stasis. 
The  latter  dejH>nds  partly  u|)on  lunv  circulatory  conditions  within 
the  kidney,  partly  upon  the  j-nulual  weakening-  of  the  jieneral 
systemic  senile  circulation.  The  re.sults  of  .such  a  Ioii<!;-continued 
.stasis  are  here  similar  to  tho.se  which  we  met  l)efore,  namely, 
dilatation  of  all  vascular  district.s,  includin<t  the  newly  formed 
capillaries  withiji  the  fibrous  tissue,  further  interference  with  the 
nutrition  of  the  parts  still  intact,  and  a  firad\ial  .serous  imbibition 
of  the  tissues,  particularly  marked  in  the  meduUary  portious. 

'J'lie  kidney,  therefore,  l>ecomes  (edematous.  Its  fjeneral 
ap{x>arance  is  hazy;  the  markinjis  iKH-ome  disturl)ed  and  less 
distinct.  It  is  for  these  reasons  that  kidneys  in  such  a  stajie  are 
frecpiently.  l)Ut  wronjiiy,  sj)oken  of  as  nephrites,  and  not  in- 
fretpiently  such  kidneys  are  rejiarded  as  an  inflanmiaton,' 
exacerbation  of  contracted  kidneys.  Hut,  as  you  see  from  the 
short  description  of  its  j)atho<ienesis,  it  repre.sents  the  late  results 
of  a  loiifi-continued  venous  coiifiestion  sujjeradded  on  non- 
inflannuatory  luitritive  disturbances. 

Hut  the  picture  may  l)ecome  still  more  complicated;  for  the 
arteriosclerotic  pntcess  frecjuently  leads  to  complete  obstruction 
of  the  larjicr  vessels,  necessarily  followed  by  infarctions.  The.se 
infarcts,  which  occasionally  are  of  considerable  majinitude,  heal 
with  the  formation  of  (leei)ly  retractinjr  sears.  It  is  herein  that 
this  kidney  differs  particularly  from  the  pure  types  of  productive 
nephritis,  and  it  jiives  the  orjian  a  coarsely  jiraiuilar  surface. 
It  is  the  type  of  kidney  which  led  (lull  and  Sutton  to  their  view.s 
about   the  Jjalhojictiesis  of  nejjhritis. 


PROnrCTIVK  XKPHHITIS.       VISCKRAI.  CHANOKS.      (KI)KMA      177 

Finally,  I  should  mention  that  it  must  l)e  considered  doubtful 
whether  all  the  atrophic  chanjies  observed  in  the  senile  kidneys  - 
and  that  applies  in  general  to  all  senile  orjians  only  and 
absoluni.  (le{)end  upon  the  (juantitative  influence  of  arterial 
changes  Xo  doubt,  these  are  extremely  important.  There  are, 
however,  certain  evidences,  the  discussion  of  which  lies  outside  the 
scope  of  these  lectures,  which  seem  to  indicate  that  senile  atrophy 
of  cells  cannot  l)e  entirely  ascril)ed  to  the  chanjjes  within  the  cir- 
culatory- apparatus,  but  include  certain  other  qualities  inherent 
to  cell  life.  Indeed,  we  observe  some  senile  kidneys  without 
much  arteriosclerotic  coar.se  contraction,  but  a  rather  uniform, 
simple  loss  of  -secretinji  substance,  the  surface  remaininjj;  smooth. 

A  characteristic  feature  of  this  type  of  kidney,  and  already 
mentioned  in  my  second  lecture  on  the  theories  of  urinarj'  secre- 
tions, is  not  only  a  relatively,  but  ab.solutely,  larsie  pelvis,  which 
sometimes  takes  on  such  dimensions  and  appears  so  dilated  that 
it  may  properly  l)e  spoken  of  as  hydronephrosis.  This  hydrone- 
phrosis may  l)e  rej^arded  as  an  idiopathic  one,  for  the  reason  that 
it  cannot  be  attributed  to  any  coarse  mechanical  interference 
with  the  outflow  of  the  urine,  but  appears  to  l)e  due  to  a  gradual 
decline  in  the  elasticity  of  the  contractile  elements  of  the  pelvis, 
and,  iw.ssibly,  of  the  ureter.  In  some  of  these  pelves  one 
oi).serves  tlistinctly  a  disintejiration  of  the  elastic  structures, 
which  appear  either  increased  or  markedly  dimini.shed.  This 
jioint  has  considerable  practical  interest  and  bearing. 

It  is  evident  that  senile  kidney  will,  sooner  or  later  durinji 
life,  eliminate  enoujrh  kidney  substance  to  produce  symptoms  of 
renal  insufHciency.  Here  pathological  and  clinical  classifications 
have  some  difficulty  in  harmonizing,  for  a  clinician  will  neces.sarily 
l)e  satisfied  to  group  such  cases  under  the  general  category-  of 
nephritis,  while  the  i)athological  anatomist  can  surely  not  V)e 
content  with  this. 


l.*! 


ITS 


HHKiHT  S    niSKASK 


li:l 


Wo  are  now  in  a  position  to  appreciate  that  not  every  jiranu- 
lar,  cicatricial,  and  atrophic  kidney  is  a  nephritis.  It  may  result, 
as  we  .><aw  Ix'fore.  from  a  lon^i-continued  venous  cyano.sis,  and, 
as  we  find  now,  from  nutritive  disturhances  incident  to  senile 
chanjics.  liven  tlie  anaton>ical  diajiiiosis  may  here  not  always 
he  easy,  ;ind  must  l)e  made  with  thoroujrh  appreciation  of  the 
factors  which  we  have  studied.  But  the  decision  of  this  point, 
ptrticularly  in  relation  to  certain  cases  of  hypertrophy  of  the 
heart.  n>ay  become  of  the  <rreatest  clinical  importance.  (Ireat 
difficulty  may  l>e  ofTered  in  cases  when  such  kidneys  as  you 
can  readily  imajiine  become  the  .seat  of  su|M>radded  exudative 
and  dejienerative  inflammatory  conditions. 

J.et  us  return  to  the  siihject  of  productive  nephritis.  We 
have  arrived  at  the  second  (piestion  which  presented  itself  at 
the  start  of  this  chapter:  What  is  the  rehition  of  the  extreme 
parenchymatous  loss  to  the  abundant  filu-ous  ti.ssue  prolifera- 
tion? 

Here  we  step  once  more  on  very  disputed  jiroinid.  You  will 
recall  from  the  first  lecture  that  there  are  two  entirely  opjiosed 
views  on  that  subject.  It  had  l)een  Weif^ert's  idea  ajul  in  this 
he  was  essentially  supported  by  Cohnheim  and  many  otliers  - 
that  it  was  necessary  to  presuppose  a  parenchymatous  injury  in 
order  to  account  tor  the  fibrous  tissue  growth.  He  rejrarded  this 
latter,  therefore,  as  strictly  c:)mpensatory.  .\n  entirely  different 
view,  however,  w.is  enter!., ined  by  Hartels.  who  rejiarded  the 
hyjMM-plasia  of  interstitial  tissue  as  the  primary  feature  of  the 
contractc.!  kidney,  and  thus  created  the  conception  of  the  pri- 
mary interstitial  nephritis.  In  this  he  was  actively  supported  by 
Xauwerck,  who  held  that  epithelial  dejieneration  by  no  me:ins 
always  preceded  the  interstitial  inflannnatorA-  chanjies. 

Some,  like  .V.schofT.  .separate  entirely  the  connect ive-ti.ssue 
formation  from  the  inflammatory  proce.ss,  and,  extending;  the 


■-iy 
■■'i'-- 


PRODICTIVK  NKI'HRITIS.      VISCKRAI.  CHAXOKS.      (KI)KMA      179 


.  1 


views  of  Wt'i^ert .  look  upt)n  it  as  a  process  of  repair.  Tliat  fjroup 
of  invest ijrators  is  therefore  uinvillinfi  to  speak  of  productive 
nephritis  at  all.  l)iit  rejiards  all  the  various  lesions  of  proliferation 
and  production  of  new  tissue,  nuich  as  \'ircli()w  did,  as  consi- 
f/ucnns  of  the  inflainniatorv  (le<renerative  and  exudative  chanjies, 
which  form  no  part  <tf  the  inflammatory  phenomena,  hut  an 
evidence  of  healin<!;.  AschotT  discards  the  terms  of  chronic 
nephritis  and  productive  nephritis,  there^fore,  and  sj)eaks  of 
nephropathia  chronica  inflanunatoria.  By  this  he  means  a  lonjj- 
continued  disease  of  the  kidney,  orifiinatinjr  on  an  inflammatory 
hasis,  hut  having  reached  stajres  of  repair  in  various  type.-^  of 
cicatrization.  He  reco«:nizes  this  le.sion  in  three  stajres:  first, 
insufficiency;  second,  com|)ensation;  and  third,  decompensa- 
tion. 

Now,  it  is  certainly  true  that  many  of  the  so-calle<l  "  chronic 
interstitial  inflanmiations,"  representin<>  an  increase  of  fibrous 
tissue  at  the  ex|)ense  of  parenchyma,  are  not  inflammatory  at  all. 
What  is,  for  instance,  freijuently  referred  to  as  chronic  interstitial 
myocarditis  is  jjenerally  scar  formation  as  the  result  of  infarc- 
tions. Similar  illustrations  may  he  found  in  other  orjians,  and  I 
have  already  itisisted  l)efore  you  that  in  the  cyanotic  induration, 
and  in  the  senile  and  arteriosclerotic  kidney,  we  are  dealinji;  with 
nutritive  disturbances  which  are  absolutely  unrelated  to.  and 
therefore  to  l)e  separated  from,  the  inflammatory  conditions  of 
that  orjjan. 

However,  it  is  very  doubtful  whether  the  proliferation  of  cells 
and  formation  of  new  tis.sue,  which  is  characteristic  of  certain 
inflammations  and  with  which  we  are  dealinji  in  the  (juestion  of 
productive  inflammations,  can  pro|M»rly  ])e  rejtarded  (mly  as 
evidences  of  repair,  or  as  a  pure  healinjj  process.  There  are  some 
points  which  difl"erentiate  them  from  the  previously  mentioned 
fibrous  irrowth  which  results  from  nutritive  disturbances: 


if 
1 1 


II 

I! 


'^ 


ISO  hhkjut's  KISKASK 

rirst  :    Tlif  cliaiifrrs  in  the  interstitial  tissue  in  iiiHainniatoiy 
processes  are  characterized  l)y  ati  active  participation  of  compo- 
nent parts  of  this  (issue  in  tlie  (h'fense  ajiainst  th«>  inflanmiatorv 
irritant.     The  clianjies  thus  j)ro(iuce(l  difTer,  therefore,  (piantita- 
tively   and   (luaHtatively    from   those   whidi   occur  (hiring   the 
process  of  repair.     Wliile.   therefore,  .some  of  the  features  of 
repair  are  evidv  ii<  in  th<'  inflanunatory  interstitial  chanjies,  they 
liave  others  .so  clo.sdy  allied  and  acting  with  and  modifyinji  them, 
that  one  cannot  well  l)e  separated  from  the  other,     l-'iuther,  the 
close  interchanjre  between  interstitial  tissue,  parenchyma,  blood- 
vessels,   and    lymphatics   lends,    as   we   have    learned,    certain 
(jualitative    features    to    the    inflammatory    coimective-t issue 
changes  which  jro  far  beyond  those  found  in  reparative  processes. 
Second:    The  inflanunatory  iiiterstitial  i)roliferation  always 
lirows  beyond  the  limits  of  n'pair.     This  important  i)oint  had 
become  evident  even  to  Wei<iert.  who  therefore  introduced  the 
conception  of  hyiwrcompensation.  later  used  by  l-^hrlich  in  the 
elaboration  of  his  side-chain   theorA".     The   process  of   repair, 
which  is  ushen'd  in  l)y  n\itritive  tissue  distm-bances,  remains 
distinctly  limited.     Into  its  formation  enters,  as  far  as  can  1k' 
seen,  onlv  the  removal  of  the  restraint  of  tissue  tension.     This 
once  reestablished,  the  proliferation  ends  and  matures  without 
•attectinji  in  the  sli<:htest  dejirce  the  neifrhborinj:  intact,  or  even 
weakened,  tissue.     The  inflanunatory  interstitial  proliferation, 
on  the  other  hand,  by  virtue  of  its  extensive  and  less  restrained 
lirowth.  Ity  blockinjr  the  i)aths  of  mitrition  and  absor[)tion,  adds 
injury  instead  of  repair.     The  causes  for  this  nuist  undoubtedly 
be    souiiht    in    the    inflammatory    circvilatory    conditions    and 
anatomical  rearraniiement  of  the  parts,  more  comjjlex  chan«;es  of 
tissue  tension  than  in  simple  repair,  nutritive  chaufjes,  and  ctm- 
tinuance  of  certain  irritative  influences. 

Herein  lies  a  \erv  decided  dilTerence  lx^tW(M>n  pure  n^i^arative 


•RODICTIVK  NKPHHITJS.      VISCKHAI.  ('JIA\(J»:S.      0';nKMA     ISl 


Pt 


and  iiiflaiiunatorv  tissiw  growth,  and  one  which  justifies  us  in 
upholding  the  conception  of  pnxhictive  inflammation  as  distinct 
from  processes  of  repair. 

Now,  an  investipition  into  the  problem  of  the  rehition  of 
parenchymatous  loss  to  the  fibrous  tissue  formation  is  made 
extren«>ly  difTicult  l)y  the  complex  nature  of  these  changes,  and 
by  the  fact  that  it  is  rare  to  obtain  kidneys  in  such  stages  of 
incipient  nephritis  as  will  allow  definite  conclusions  on  that  point . 

It  seems,  however,  as  if  somewhat  intermediary  antl  more 
flexible  views  would  come  nearer  the  truth  than  any  one-sided 
and  ri;;id  idea:  Certain  forms  of  nephritis  are  associated  from 
the  start  with  progressive  parenchymatous  destruction.  It  ap- 
jM>ars  that  in  these  we  cannot  attribute  the  lo.ss  of  parenchyma 
to  primary-  proliferation  of  interstitial  tissue,  but  that  it  is  at  least 
concomitant,  ami  by  its  loss  does  not  opjmse  an  vmre.st rained 
connective-tissue  hyix^rplasia.  These  cases  would  conform  with 
Weifjert's  views.  On  the  other  hand,  there  exist  types  of  nejjh- 
ritis  which  originate  as  primarily  localized  ix^rivascular  infiltra- 
tions. These  localized  areas,  howev;  r,  are  rapidly  followed,  pos- 
sibly by  virtue  of  their  existence,  possibly  by  extension  of  the 
inflanunator>'  irritant,  or  both,  by  nutritive  disturbances  of  the 
involved  parts.  Pareiictiymatous  destruction,  therefore,  ensues, 
and  inaufiurates  the  possibility  of  furtlier  extension  of  the  in- 
flammator>'  infiltrations  and  connective-tissue  growth.  With 
the  stM'ond  view  we  take,  as  you  may  see,  a  .somewhat  reconcil- 
ing stand  l)etween  extreme  ideas. 

Ijet  me  now  touch  upon  some  of  the  important  functional 
characteristics  of  productive  nephritis.  One  of  the  most  inter- 
esting: is  the  strange  fact  that  throufjhout  the  course  of  this 
disease  the  urine  (|uantity  is  verA*  much  increased.  This  in- 
crease, althoufih  not  reachinj:  such  high  figures  as  in  diabetes,  is 
nevortheles.'*  considerable,  aiid,  curiously  enough,  persi.sts  toward 


1    i- 

i  I 


I  ^ 
I  I 

■ 


1S_» 


HUKiHTS    niSKAsK 


llwriul.     'riial  is  its  most  [HTplcxiuji  phniomcnoii.     No  matter 
wlu'tlicr  we  (iiid  at  autopsy  almost  all  tlw  normal  kidney  sul)- 
staiicc   ilcstroyed.    the    (piaiititativc   excretion    of    the    waters 
elements  has  remained  hi}:h  to  exitus.  unless  circulatory  dis- 
turbances or  exacerbations   complicate   the   terminal    pictun'. 
We  have  no  really  satisfactory  explanation  for  this  phencmienon. 
It    may.    of    cours<'.    Ik'    supposed    that,    particularly    at    the 
l«';iinnin;i  of  the  disease,  conjiH'nsatorj-  hyixrf unction  on  the 
part  of  the  preserved  kidney  portions  occurs;   but  how  does  it 
keep  up  as  the  kidney  substance  wastes  and  is  replaced  by  con- 
nective tissue?     It  is  here  pariicularly  that  we  must  look  for 
other  than   purely    physiolojiical   n^asons.     The   kidney   of  an 
advanced  productive  nephritis  is  really  not  comparable  to  the 
normal  orjian."     Not  only,  as  you  rememln'r,  has  there  taken 
place  far-reachinji  chan-tes  in  the  vascular  supply  and  secretin}! 
chamiels,  l)Ut  the  epithelium  has,  as  you  also  recall,  chanjied  its 
type  entirely.     From  a  hifihly  differentiated,  six>cialize(l  form, 
it  has  either  k'come  cylindrical  or  more  fretiuently  descended 
further    to    an    endothelial,    syncytial-like    formation.     These 
atypical  forms  of  epithelimn  receive  their  blood,  by  elimination 
of  most  <:lomeruli,  in  uimiodified,   unccmcent rated  form.     It   is 
evident   that   this  complete   reor<ianization   of   parts   must    W 
followed  In-  far-r(>achin<r   effects.     In   the  same   way   we  may 
possii)ly  account  for  thejiradual  less(Mied  concentration  of  such 
urines,  which,  althoujih  frecjuently  very  hi«ih  in  the  iK'f-inninji, 
l)ecome  lower  in  specific  jiravity,  until  toward  the  end  the  ex- 
cretion of  solids,  in  spite  of  an  abundance  of  urine  water,  is  far 
Ix'low  any  normal  figure. 

In  other  words,  the  late  n)anifestations  in  the  functional 
deranj^ement  of  this  tyi)e  of  nephritis  .seem  to  dejx^nd  on 
new  structural  forms  and  arran<:ement,  which  are  not  comparable 
to  the  phy.siolof;tcal.     The  orjjan  is  a  new  functionatinj!  unit. 


i  I 


IMIODI  ( TIVK  NKI'HKITIS.      VISCKHAI,  CHAXtiKS.      (KDK.MA     \H'.\ 

If  yovi  have  followed  the  morpholojiical  chaiinr.s  carefully, 
you  will  readily  see  that  the  urine  in  the  pun-  ty|H's<>f  productive 
nephritis  nuist  l»e  |M)or  in  niorphotic  elements  and  seruni- 
all»uniin.  I)<'st ruction  of  kidney  suhstance  is  ver>-  slow,  cer- 
tainly never  intense,  and  wide-spread,  rapid  desquamation  of 
epithelium,  and  the  formation  of  nuich  inflannnatory  detritus 
and  active  diffusi'  exudation  heinjr  lacking.  A  moderate  num- 
U'r  of  hyaliiH".  occasional  firanular  and  fatty  casts,  often  found 
only  after  consideralde  centrifufjinn,  and  occasional  leukocytes, 
an'  therefore  the  only  elements  found.  Serum-alhumin  exists 
only  in  traces,  except  where  the  lesion  is  complicated  l)v  amyloid 
defieneration. 

Herewith  we  have  fini.shed  our  pro|)osed  work  the  considera- 
tion of  the  pathological  an.itomy  and  histolojiy  of  Bri^ht's 
disease  as  far  as  the  kidneys  themselves  nrv  concerned.  From 
the  mass  of  evidence  and  known  facts,  it  has  l)een  my  endeti 
to  select  the  most  important,  not  presentiiiii  them  as  inde|)ende. 
or  incoherent  de.scriptions  and  statements,  but  moldinj:  them 
into  a  plastic  form  which  will  allow  you  to  form  visual  pictures 
and  relations  of  the  nephritic  proces.ses. 

In  conclusion,  however,  I  must  touch  upon  some  featui-es  of 
nephritis  which,  although  lyinji  outside  of  the  kidney,  are  really 
part  of  the  jjeneral  mori)holo{rical  consideration  of  the  subject. 
First .  chaiifies  in  some  other  viscera;  and.  .secondly,  the  ques- 
tion of  cedema.  These  are  so  inijiortant  and  characteristic  that 
we  cannot  well  omit  them.  Of  the  chanjies  in  the  viscera  we 
immediately  re<'  )>inize  those  of  the  heart  as  the  best  known  and 
very  important.  That  any  nephritis  which  extends  over  a 
lonfier  jx^riod  may  In^come  associated  with  a  hyf)ertrophy  of  the 
heart  was  known  to  Brifrht,  and  so  overwhelminji  has  l)een  the 
evidence  .since  his  first  observations,  that  this  is  one  of  the  best 
accepted  complications  of  nephritis.     While  the  carefully  tabu- 


!i 


I      I 

n 


IS  I 


UIIKiriT  S    DISKVSK 


latcd  oliMTViitioiis  of  MiiiiilH'i-jjrr  and  TriiuU'  and  ji«'U<'ral  v\- 
|H'ri('iic»'  <>iii|)|)asiz«'*l  the  |)n>|M)ii(lcraii*'(>  of  tlir'  hy|N>rlr()|>hy  of  the 
left  ventricle,  it  is  really  only  very  recently  that  indisputable 
evidence  lias  iK'en  furnished  alntut  the  niaiUHT  under  which  the 
heart  hy|H'rtrophies  in  nephritis.  By  can'ful  weifrhiii);.  aci'ord- 
iii^  to  W.  Miiller's  method,  l{oinlN>rv;.  llasiMifeld.  and  llirsch 
have  denionst rated  that  in  .S2  jht  cent,  of  their  ca.s<>s  all  cavities 
of  the  heart,  auricles  and  ventricles,  show  hy|)ertr(>phy  of  their 
walls.  The  left  ventricle,  howevj'r.  pre.s<'iits  this  most  markedly. 
In  14  |H'r  cent  only  the  left  ventricle  was  hy|n*rtrophied.'"' 
Hirsch  demonstrated  that  tin*  hyixTtrophy  of  auricles  and  the 
ri<tht  ventricle  follows  that  of  the  left  ver»t rich',  and  Piisslerthat 
the  rijiht  side  (»nly  hy|M'rtrophies  when  the  left  side  Ix'coines 
insuthcient. 

These  fijiures  are  accepted  by  Kn'hl  as  perfectly  conclasivo. 
They  are,  however,  as  now  all  patholojiists  and  clinicians  know, 
open  to  som<>  variations. 

In  the  first  place,  it  is  well  settled  that  hyj)ertrophy  of  the 
heart  occurs  only  in  thos*^  ca.ses  which  are  as-sociated  with  an 
appreciable  rise  in  l)lood-pres.sure.  It  is,  therefore,  not  abso- 
lutely dejM'ndent  upon  or  associated  with  any  particular  kind 
of  nephritis.  While  it  is  most  constant  in  the  bruscpie  exudative 
ty|M's,  particularly  tho.se  with  marked  vascular  injury,  as  in 
scarlet  fever,  and  in  the  productive  forms,  it  may,  nevertheless, 
l)e  al)sent  in  all  of  them  for  the  followinjj  rea.sons:  The  factors 
leadinj:  to  increased  blood-pre.ssure  may  Ix'  lackinj;;  or  the  or- 
jianism  may  1k'  unal)le  to  resjK)nd  to  the.se  factors;  lastly,  a 
once  estal)lished  hyjK'rtrophy  may  .^ive  way  to  later  atrophy. 
The  latter  two  features  are  imiM)rtant  to  rememU'r,  and  have 
been  fully  tlemonstrated  by  our  own  ecords.  The  hyper- 
trophy then  occurs  and  jK'rsists  only  when  the  nutrition  of  the 
orjiun  is  kept  up  to  the  r!?cess;ir\-  stantlard. 


j? 


PHODICTIVK  NKI'HHITIs.       VISCKHAI.  «ll  %\(iM.      (KDKMA     IH') 

Sj'niitor,'"  Honio  yourH  a^'".  |H)inli*(l  out  that  ntw  coul*!  diffor- 
f'litiato  iH'twrcn  two  foriiis  of  hyixTtntpliy :  oin'  with  dilatation 
of  thr  ventricle,  the  so-(alle<l  eccentric;  and  one  without  dilata- 
tion, simple  or  concentric.    He  conchuled  fn)in  his  ol)s<'rvalions 
the  occurnMice  of  the  first  in  the  larjie,  dej;en«'rative,  exudativ«'. 
fatty,  and  hemorrhagic  nephrites,  wliile  the  latter  was  the  rule 
in  the  small,  contracted,  productive  forms.    This  view  was  s<M)n 
op|M)s«Ml  from  many   exceptions   liy   ('«»hnheim   and    later  ol»- 
servations.    amonjj    which    I    have    made   a    niunln'r    myself. 
Thes*'  «lemonst rated  the  dejx'ndence  of  eccentric  or  concentric 
hy|)ertrophy  u|X)n  the  jjeneral  nutrition  of  the  individual.     In 
the  degenerative  exudative  nephrites  with  much  (edema  and 
hydrops,  the  nutrition  of  the  individual  and  of  the  heart  nmsde, 
particularly  toward  the  enu.     iffers  severely;  naturally,  we  find 
at  autopsy  dilated  ventricle^,  on  the  other  hand,  in  the  slowly 
projiressinj;  uncomplicated  pnxluctive  nephritis,  the  iiutrition 
usually  remains  ver>-  jjood  till  toward  the  end.    Here  concentric 
hy|)ertrophy  is  then'fore  moiv  freipiently  foimd.     An  absolute 
de|x^ndence  of  any  form  u{)on  a  particular  kidney  lesion  does 
therefoH'  not  seem  to  exist.'" 

Now.  how  is  this  hyi)ertrophy  to  lye  interpreted?  Bri<;ht 
held  to  two  jM)ssil)ilities:  luther  the  heart  is  directly  irritated  hy 
an  abnormal  composition  of  the  bl(K)d,  or  this  affects  the  finer 
and  capillary  vessels,  thereby  aujimentin<>;  the  work  of  the  heart 
in  order  to  drive  blood  throu^jh  thus  affected  vascular  districts. 

The  immediate  successors  of  Bright  in  the  study  of  renal 
disease  did  not  further  our  knowledjje  refjardin^  this  matter, 
until  the  work  of  Traulx*"*  gave  a  new  stimulus  to  it.  Traube 
showed  during;  life  that  within  a  few  weeks  after  the  occurrence 
of  a  severe  nephritis  symptoms  appeared  which  pointed  toward 
increased  tension  in  the  aortic  system.  These  are  abnormal 
resistance  of  the  radials  and  the  apex-l)oat,  and  j'n  accentuated, 


i 
1 


1S(> 


HHICHT  S    niSKASK 


liijlh-souiuliiij:,  diastolic  aortii-  and  carotid  tone.  To  thorn  is 
addod  soon  an  increase  in  the  heart  vohnne,  and  Tranl)e  (h>mon- 
strated  in  some  cases  hypertrophy  of  the  heart  in  as  short  a  'inie 
as  four  weeks  after  the  l»e,iiiiniinfi  of  a  nej)hritis. 

In  this  way  he  conchided  a  causal  relation  between  nephritis 
and  hypertrophy  of  the  heart,  and  assumed  for  its  explanation 
the  followinjr: 

First :  Infianunatory  lesions  of  the  kidney  cause,  hy  presence 
of  an  exudate  or  l)y  loss  of  kidney  substance,  a  diminution  in  the 
amount  of  fluid  al)stracted  from  the  aortic  system  for  the  pro- 
duction of  urine  water.  Second:  They  diminish  the  quality 
of  blood  which  in  a  jriven  time  flows  from  the  aortic  to  the  venous 
system. 

This  purely  mechanical  liypothesis  was  soon  attacked  for 
physiolo<:ical  and  j)atholojiical  reasons.  It  was  demonstrated 
by  Cohnheim  and  Lichtheim  ''  that  a  hydremic  plethora  has 
al).solutely  no  influence  on  the  blood-pressure,  and  by  Ludwij; 
and  his  pupils  that  even  tyin<;  of  both  renal  arteries  had  no 
appreciable  etTect  on  it.  Furthermore,  it  is  well  known  that, 
particularly  in  the  productive  nej)hrites,  tlie  amount  of  urine 
vvater  is  not  only  not  dimini.shed,  but  actually  increa.sed.  Never- 
theless, this  mechanical  theory  was  championerl  l)y  Cohnheim 
in  modified  form,  l.ariiely  for  the  rea.son  that  exjH'rnnentally  and 
clinically  left-sided  hyjwrtropliy  follows  total  extirpation  of  one 
or  jrradual  elimination  of  both  kidneys,  notably  exemplified  in 
cases  of  uncomplicated  hydronephrosis.  Lack  of  occurrence  of 
hypertr(>phy  under  (he.se  conditions,  and  in  amyloid  kidney,  was 
attributed  l)y  ("ohnheim  to  purely  nutritive  disturbances.  In 
order  to  meet  the  previously  mentioned  ol)jections  to  Traube'.s 
theories,  Cohnheim  supi)o.se  1  that  the  rise  in  pressure  was  due, 
first,  to  entrance  of  an  unchanired  amount  of  blood  into  the  kid- 
neys,   where    it    meets   increased    resistance,    and,    s(^cond,    an 


PKODrCTIVK  XKPHUITIS.       VISCKHAI.  CHANCKS.      <KI)KMA     187 

almost  normal  ([uantity  of  urinous  suhstaticos,  which  determine, 
in  his  opinion,  the  decree  of  contract ihility  of  the  smaller  renal 
vessels.  In  otlier  words,  ("ohnheim  l)elieved  that  the  amount  of 
l)lood  entcrinfi  the  smaller  kidney  arteries,  whose  contractive 
state  is  determined  hy  the  quantity  of  urinous  substances, 
remains  constant.  Beyond  these,  however,  it  meets  the  in- 
creased resistance  which  necessarily  leads  to  increase  in  -ieneral 
arterial  tension. 

This  theory,  like  Trauhe's,  has  not  enjoyed  jjeneral  recojini- 
tion.  Senator  -"  h:is  pointed  out  that  the  smaller  kidney  vessels 
are,  as  a  rule,  distinctly  diseased,  so  that  the  conception  ad- 
vanced by  ("ohnheim  se(>ms  unreasonable.  For  Krehl -'  and 
others  it  is  im{)ossil)le  to  understand  how  elimination  of  a 
relatively  small  area  of  circulation  should  be  followed  by  such 
a  jwrmanent  rise  in  sieneral  blood-pressure,  and  not  by  compen- 
satory dilatation  in  other  districts,  a  fact  which  is  t!ie  rule  in 
other  conditions,  finally  there  is  no  direct  relation  between  the 
ext(>nt  of  hypcTtrophy  and  the  defjrec'  of  kidney  contraction. 

Schmidt,--'  who  ditTerentiates  l)etween  two  kinds  of  nephritis, 
fllomerulonephritis  and  pure  parenchymatous  tyi)es.  in  which  I 
am  unable  to  follow  him.  lH>lieves  that  the  affection  of  the  jilomer- 
uli  is  of  jireatest  importance  in  the  rise  in  tension  and  ultimate 
hypertrophy,  althoujih  intensity  and  jrenerality  of  tlie  <rlomerular 
lesions  do  not  seem  lo  have  any  relation.  Schmidt  l)elieves, 
therefore,  that  the  whole  is  a  reflex  process,  actinj:,  not  on  the 
heart  directly,  but  on  the  smaller  arteries.  But,  inasmuch  as  I 
have  never  seen  any  nephritis  without  jrlomerular  lesions,  I  can- 
not support  any  of  his  contentions.  But  firantinj:  it,  one  cannot 
see  why  the  blood-pre.ssure  is  so  extremely  hijjh  in  late  sta}z;es  of 
productive  nephritis,  when  <>;lomeruli  have  larjiely  di.sappeared ; 
and  why  nuidi  lower  in  the  fatty  dejienerative  type,  where  glom- 
eruli are  still  {wrsistent  and  jienerally  diseased. 


i 


INS 


HHKillT  S    DISKASK 


By  far  tho  larjiost  jiuiiiIkt  of  invest ijiators  look  for  tl 


11'  cause 


of  hijrli  tension  and  hyjHTtrophy  of  tiie  heart  outside  of  tiie  kid- 
ney. One  uroup  of  ideas  finds  the  exphmation  in  chanjies  of  the 
arterial  system.  To  them,  rise  in  l)loo<l-pre.;sure  and  hy|K>r- 
trophy  of  the  heart  is  not  dependent  upoji.  hut  associated  with, 
the  nephritis.  The  ideas  of  Cull  and  Sutton,  and  others,  on 
••arterioeapillary  tihrosis."  form  the  foundation  for  these  views. 
\\v  have  previously  studied  the  arterial  changes  in  the  kidney, 
and  those  of  th(>  other  arteries  outside  of  the  kidney  are  verA- 
similar.  .Many,  as  we  saw.  are  not  the  cau.se  of,  init  actually 
dejK'udent  on.  the  rise  of  hlood-jH-es.-;;,'  and  the  heart  hyix>r- 
troj)hy.  Furthermore,  the  occurrence  of  arteriosclerosis  in 
nephritis  varies  .so  nnich.  and  frecjuently  in  .severe  cases  with 
much  hypertrophy  in  the  youn-i  is  .so  conspicuously  ah.sent,  that 
we  cannot  l)rin^  it  in  any  essential  relation  to  the  hypertrophy. 
Some  time  a-io  the  question  of  splanchnic  arteriosclerosis  as 
cause  for  hijih  hlood-pre.ssure  was  much  discussed.  It  was 
tlK.ujiht  that,  althctujrh  the  larjier  alxloininal  vessels  mijiht  not 
show  marked  lesions,  .smaller  arteries  o*"  the  abdominal  orjtans 
in  spleen,  liver.  i)ancreas.  <iut.  etc..  presented  sufficiently  far- 
reachinji  arterial  narrowinji  to  account  for  ri.se  of  nephritic 
hlood-pre.ssure.  I  have  paid  .some  attention  to  this  my.self, 
hut  have  heen  unahle  to  trace  any  satisfactory  relation  between 
splanchnic  arterio.sclerosis  and  rise  in  bl()od-pres.sure. 

Kwald-'  considered  that  an  increased  internal  friction  of  the 
blood  mijiht  .account  for  the  hypertrophy,  but  Hirschand  Beck-' 
found  the  viscosity  of  the  blood  not  increase*!  in  nephritis. 

liy  far  the  larjie.st  niunber  of  inxesti-rators.  and  even  Bri<rht, 
have  accepted  on(>  or  the  other  chemical  or  toxic  explanation  of 
ri.s(>  of  blood-pre.ssure  with  hyjK'rtrophy  of  the  heart.  We  owe 
to  Senator-"'  an  exceedinjily  well-formulated  expression  of  this 
view,  and  the  ideas  of  other  investigators  alonjr  these  lines  may 


I'KODICTIVK  NKPHHITIS.       VISCKH  \L  CHANtiKS.      (KI)KMA      1S9 

well  \ic  rpfianled  as  modifications  of  Senator's  ori^jinal  coiiocp- 
tion.     In  tlie  first  place,  he  holds  that  somewhat  different  factors 
are  potent  in  produciiif;;  hypertrophy  of  the  heart  in  various 
forms    of    nephritis.     In    what    he    terms    "  parenchymatous, 
nephritis,"  and  whfit  we  call  degenerative  exudative  nephritis, 
the  kidney  and  the  whole  orjianism  are  exposed  to  an  irritant, 
which  therefore  acts  on  heart  and  blood-vessels  as  well  as  on 
kidneys,  and  produces  primarily  mlema.     The  latter   process 
HMnoves  some  of  the  toxic  irritants  from  the  circulation.     If  the 
lesion  thus  ameliorates,  a  neces.sarily  somewhat  weaker  but  per- 
sistent irr  tant  continues  a  vasocontraction.  followed  by  thicken- 
inji  of  ttie  vessels.     Simultaneously,  this  irritant  acts  on  the 
heart    rnusde.     The  heart  muscle  hypertrophies,  therefore,  for 
two  reasons:  First,  as  the  result  of  an  increased  resistance;  and, 
secondly,   as  the  direct   result   of  an  irritant.     These  are  the 
responsible  factors,  accordinjr  to  Senator,  in  what  he  terms  the 
chronic  parenchymatous  and  secondar>-  contracted  kidneys- 
conditions  which  we  called  dej-enerative  exudative  and  dejiener- 
ative  productive  nephrites.     In  the  primary-  productive  neph- 
ritis, on  the  other  hand,  the  irritant,  althoujih  constant,  is  never 
stronjr  enoufih  to  lead  to  hydrops  or  anlema.  but  produces  here 
also  contraction  of  smaller  arteries,  which  is  necessarily  followed 
i)y  hyi)ertrophy,  particularly  of  the  left  ventricle.     Under  both 
conditions,  then,  a  .similiir  resultinj>;  nicreased   pn^ssure  in   the 
aortic  system  occurs:     These  ideas  were  actually  supported  l..- 
experimetital   oi)servations   which   showed   a   transient    rise   in 
blood-pressure  after  injection  of  urea,  althoujrh  Senator  himst^lf 
is  inclined  to  attribute  an  even  j:reater  influence  to  the  other 
nitrofienous  waste-products. 

This  theory  is  very  in-jenious.  i)articularly  as  it  accounts  not 
only  for  the  rise  in  blood-pressure  and  hypertrophy  of  the  heart, 
but  brinjts  these  at  once  in  a  relation  with  the  (edema  of  nephritis. 


1«>U 


HHKJHT  S    niSKASK 


As  I  told  you.  the  main  principles  of  this  toxic  thcon-  have  now 
Ik'cii  iiciicrally  accepted.  Krehl's  idea,  which  is  somewhat 
simpler,  is  that  the  contracti(»n  of  the  smaller  arteries  is  tiie  most 
important  factor,  and  that  this  is  not  to  he  rejiarded  as  a  spasm 
of  these  vessels.  i>ut  rather  as  an  increased  tonicity  of  the  normal 
vascular  tone,  which  is  probably  under  th(>  influence  of  definite 
nervous  vascular  centers.  A  discu.ssion  of  these  clinical  features 
of  hi^h  blood-pressure  will  be  found  in  T.  ('.  Janewav's  niono- 
liraph  on  the  subject.''' 

A<rainst  these  ideas  it  was  ajrain  ur<ied  by  Cohnheim  that  they 
are  dealin-r  with  hypothetical  substances,  about  the  existence  and 
action  of  which  we  have  neither  proof  nor  any  knowledjie;  and. 
secondly,  that  in  the  early  stajics  of  productive  nephritis,  when 
lh(>  secret  i(»n  of  solids  and  urine  water  is  not  oidy  not  diminished, 
but  actively  increased,  the  arterial  tension  is  very  hijih  and 
the  circulatory  evidences  appear  freipiently  before  any  of  the 
renal  lesions  becoin<'  manifest.  The  ret(>ntion  of  urinary  pro- 
ducts, to  which  Senator  attributed  the  toxic  vascular  con- 
traction, nnist.  accordinu  to  Cohnheim.  be  therefore  out  of  (pies- 
tion. 

I.  too.  am  of  the  opinion  that  in  dilTerent  forms  of  nei)hrites 
different  factors  enter  into  the  production  of  rise  in  blood- 
pressure  hypertrophy  of  the  heart,  and  some  of  these  are  to  l)e 
found  outside  of.  .Mud  some  within,  the  kidney.  In  the  first 
place,  it  appears  i.rol)able  that  in  the  early  sta-ics  of  productive 
nephritis  a  toxic  factor  must  be(»f  <ireat  issue.  This,  as  evid(>nce 
indicates,  camiot  be  a  retained  normal  urinar\-  product,  or 
products,  for  circulatory  cliaiiiics  occur  at  an  early  date  when 
retention  of  urine  and  solids  is  not  only  not  diminished,  but 
increased.  It  is.  therefore,  more  prob;d)Ie  to  rej>;u-d  it  as  an 
abnormal  either  infective  or  metabolic  poison,  which  increases, 
as  Krehl  su-r'iests.  the  tonicity  of  all  l)lood-ves.sels  within  and 


I'HODICTIVK  NKl'HKITIS.       VISCKKAI,  CHANCKS.      (EI)EMA     191 

outside  of  tho  kidney  in  |)enn:uient  fashion,  k'a(Un<r  to  rise  in 
l)loo(l-pr('ssuro,  hyi)ertrophy  of  the  heart,  and  a  firadual  waste 
of  kidney  svil)stance.  The  whole  process  then  increased  blood- 
I)ressiire,  hypertrophy  of  the  lieart,  and  nephritis  stands  in 
correlation  as  the  result  of  the  injury  of  a  foreifjn  invasion  and 
their  effort  to  eliminate  it  from  the  system.  Now.  as  the  kulney 
.sul)stance  wa.stes.  certain  new  complicatinji  factors  are  intro- 
duced on  the  part  of  the  entirely  chanjred  circulatory  conditions, 
and  we  inuy  rcjiard  here,  althoush  modified  from  Traube  and 
Cohnheim.  a  certain  k)cal  influence.  This  has  only  lately  been 
once  more  emphasized,  so  that  I  do  not  feel  justified  in  deny- 
inji  it  all  importance,  as  some  would  have  it. 

We  have,  as  Cohnheim  held,  anatomical  observations  which 

indicate  that    elimination   of  the    circulation  of  the  kidney  is 

actuallv   followed   by  hypertrophy  of   the   heart,   and  further 

experimental  work  has  ajtain  turned  our  attention  to  the  ideas 

of  Traul)e  and  ("ohnheim.     Thoma   found,  some  time  aj-o,  in 

his  experiments  on   the   circulation   in   contracted   kidneys,   a 

very    appreciable    resistance    within    the    kkliiey    di.striv-t,  and 

Katzenstein  has  endeavored   to  prove  that  Cohnheim's   reply 

to  Ludwiji's  objection  to  Traube's  theory  was  actually  correct. 

Katzenstein'"  showe<l  that,  while  Ludwiji  and  his  pupils  were 

ri^dlt  in  the  ol)serv:ition  that  tyinji  of  both  renal  arteries  outside 

of  the  kidneys,  or  at  the  liilus.  was  foUowed  by  no  rise,  but  even 

a  fall  in  blood-pre.ssur(>.  thinjjs  difTered  when  the  resistance  was 

introduce<l.  while  the  renal  circulation  remained  in  coimection 

with  the  aortic  one.     If  the  renal  circulation  was  resununl  after 

havinjr  tied  the  renal  artery  for  a  lon<:  enoufjli  time  to  obtain 

thrombosis  in  the  ves-scls  of  the  kidney,  a  very  appi-eciable  rise 

occurred  and  lasted  several  hours.     These  experiments  corrolw- 

rate<l  some  results  pnniously  recorded  by  Oscar  Israel,-'  who 

obtained  rise  in  blood-pressin-e  after  extirpation  of  both  kidneys 


l!)L' 


MI<I(;ilT  S    DISKASi; 


m  fifteen  niMiits,  ami  are  {wrhaps  less  ohjectioriahle,  U'eause  an 
influence  of  urinary  substances  caiuiot  have  been  active. 

It  seems,  therefore,  that  we  cannot  entirely  (ii.siniss  the  claims 
of  TraulH'  and  Colinheim  that  certain  anatoniical  and  ex|x>ri- 
menlal  evidence  points  to  the  fact  that  resistance  within  the  renal 
circulation  may  have  an  effect  on  jreneral  blood-pressure,  and, 
therefore,  if  not  the  origin  of  hi^h  bloo(l-pres.><ure,  contributing 
toward  its  maintenance.* 

This  factor,  moreover,  seems  toaccoiuit  for  the  rise  in  blood- 
pressure  which  occurs  in  chronic  venous  conjiestion.  In  the 
various  forms  of  deireiuTative  and  exudative  nephrites,  however, 
it  is  po.ssible  to  conceive  the  coexi.stence  of  toxic  and  local  condi- 
tions. In  the  later  stajres  of  these  nephrites  the  waste  of  kidney 
substance,  the  new  arranjrement  of  the  parts,  elimination  of 
iilomeruli  and  other  vascular  chaimels  within  the  kidney,  may 
Lcradually  add  increasin<:  momentum  to  the  local  factor,  while 
the  occurrence  of  ura>mic  manifestations,  with  sudden,  some- 
times tremendous,  rises  in  blood-pre.ssure.  would  indicate  here 
also  the  jwrsistence  of  the  toxic  influence,  which,  after  consid- 
erable accumulation,  suddenlv  rises  to  exert  an  overwhelmin<i 
effect . 

To  the.s<>  a-rents  must  Anally  !«>  added,  in  some  cas(>s  at  least, 
a  jrradually  increasini:  rigidity  of  all  blood-vess<>ls.  which  is 
attril)ut;!ble  to  the  loiiii-coiitinued  increase  in  their  tonicity  and 
their  jrradu;il  thickenin.i,^ 

In  this  connection  a  few  words  ;ii)out  th(>  relati(mship  of  the 
suprarenal  irlaiids  to  blood-pivssure  and  hypertrophy  of  the 
heart:  Heceiitly  some  observers.-"'  particularly  anK)njj;  the 
l"rench.  have  claimed  that  in  lonjr-contiiiued  nephrites  with  hijih 

*riH(|iicslioM  wliillicr  tlii-  i>  .liic   t,)  .1  ri'lIcK  i,r  i •Ii;,iiir;i|   art    is  still   misi-ttlcil 

1  rc.frssnr  >,;t:,\„r  |„|,|  i,,,.  I:ili-I.v  lliut  iii  rci-cMl  .■xpcniiicnts  ti,.  ;im,1  othns  >vcr.>  iiiiiiMc  to 
iil)t;ilii  tins  rise  i!i  l>l(««l-|)rissiiii'  if  ;iiimmls  were  ilfi-piv  iiaridtizccl.  This  \  .iM  uricuc  of 
course,  anaiiist  a  iiiiTliaiiical  faclor. 


I'UonrCTIVK  NKl'HHITIS.       VISCKKAI.  CHANCKS.      (KDKMA      19Ii 


hlood-prpssurc  a  hyjKTplasia  of  the  suprarenal  inedulla  occurs, 
while  the  "ortex  also  shows  nodular,  adenomatous  hypertrophy. 
This  is  l)rou<iht  in  relation  to  hijih  blood-pressure  as  an  expres- 
sion of  functional  hy|H'ractivity  of  these  parts,  mainly  on  the 
strength  of  the  physiolo<;ical  exjx'rieiu-.^  that  a  hlood-raisinj: 
principle  may  Ix'  obtained  from  the  medulla  of  the  suprarenal 
fjland,  while  a  detoxicatin^  jM)wer  is  a.scribetl  to  its  cortex.  It 
would  lead  me  here  too  far  to  j:o  into  an  elaborate  di.scussion  of 
the  whole  matter,  but  I  would  simply  mention  that  we  have 
l)een  unable  in  this  uistitute  to  corroborate*  those  ideas,  and, 
indeed,  I  should,  from  our  ex{)erience,  conclude  that  j^eneral 
atrophy  of  the  cortex  was  a  very  j)r()minent  phenomenon  in 
nephritis.  The  state  of  the  .suprarenal  inedulla  varies  so  decid- 
edly that  it  has  not  Xah'u  {)<)s.sil)le  for  us  to  brini;  it  into  any  rela- 
tion to  the  nephritij-  process. 

Of  fireat  importance  are  the  chaiifies  in  the  serous  membranes, 
not  only  on  account  of  their  practical  interest,  but  Inn-ause  they 
throw  some  li;;ht  on  the  jjenesis  of  cedema  and  hydrops,  which  we 
shall  lastly  liave  to  con.sider. 

It  has  Ix'en  a  common  exj)erience  that  nephritics  are  .seriously 
threatened  with  inflammations  of  their  serous  membranes.  Of 
these,  it  is  particularly  the  pt^ricardium ;  then,  in  order  of  fre- 
(juency,  the  pleura,  the  jx^ritoneum,  and  finally  the  meninf!;es. 
So  frequent  is  the  combination  of  pericarditis  and  nephritis  in 
our  experience  that  when  we  find  recent  fibrinous  or  purulent 
{)ericarditis  at  autopsy,  we  immediately  exjx'ct  to  disclo.se  later  a 
ne{)hritis.  The  same  holds  true  of  fibrinous  or  purulent  jx'ri- 
tonitis,  iind  it  occasionally  hapix>ns  that  such  patients  aic  oix^r- 
ated  upon,  l)ecause  duriiifi;  life  an  appendicitis  or  other  localized 
peritoneal  infection  is  suspected.  This  conunon  involvement  of 
the  serous  membranes  was,  as  you  will  recall,  known  even  to 
Bright  and  Christison      It  is  usually  considered  that  the  cause 

14 


MM 


HliKillT  S    DISKASK 


for  such  tciiiiiii;il  iiifcctious  lies  in  flic  Icssciictl  resistance  of  tlie 
intlivi<lu;il  ms  the  result  of  loiiii-continned  nephritic  inlo\ic;itions. 
Itut  if  we  e\;iniine  the  niiilter  cMrefiilly,  :in<l  why  p.irticuhirly  the 
serous  ineiul)r;mes  ;ire  thus  so  easily  afTiM-led.  we  lintl  that  these 
have  almost  always  heen  the  seat  of  previous  produi-tive  ami 
atr(t|)hic  inllammations.  It  is  one  of  the  coinnionest  autopsv 
findiniis  in  iiei)hritis  to  see  the  serous  inemhraiies  in  parts  thick- 
ened, either  dilVuse.  uivint;  to  the  whole  a  white,  shiny,  pearly 
ap}M'arance.  or  only  circumscrilied:  in  others  thin  and  wasted, 
deformed,  adherent.  .Most  interestin^i  is  the  ac<-(,mpanyin,!j: 
|>roductive  lymphauiritis.  The  thickened,  partlv  ohliterafed 
lymphatic  vessels  stand  out  very  prominently  in  the  form  of 
|)ale,  milky-white  streaks,  formin;;  an  irreiiular  network,  and, 
in  places,  accompanied  l»y  a  perilvmphaiiiiitis,  hecome  confluent 
to  form  smaller  and  l.arjicr  patch(>s. 

ihese  latter  lesions  are  usually  well  ai-centuated  and  easily 
observed  in  the  reflected  visceral  jMMitoneum,  hut  can  also  1m> 
seen  in  pericardium,  meninjics,  and  pleura.  From  this  exjM'H- 
eiK-e  it  may  Im'  concluded  that  the  productive  inflannnations  of 
all  serous  memhranes.  which  often  iK>come  a.s.s()('iated  with  serous, 
fibrinous,  and  (>ven  purulent  exudations,  are  the  result  and  ex- 
pression of  a  jicneral  irritant  to  the  lymphatic  .system  in  nephritis. 
It  leads  us  directly  lo  the  causes  of  (edema  and  hydrops,  a  field 
which  has  for  years  heen  one  of  the  most  fruitful  forex[)enmental 
patholouy. 

For  a  full  discu.ssion  of  the  early  works  and  thoujihts  in  the 
matter  I  refer  you  t<»  the  masterly  presentation  and  criticisms 
of  Cohnheim  in  the  first  volume  of  his  lectures  on  jiencral  Path- 
olofiv,  S<M-tion  ^'U,  on  Hydriemia  aiid  Anhydra-mia.  Recently 
the  matter  lias  heen  excellently  di.scu.ssed  l»y  Meltzer  (  n  the 
vitalistic,  and  Starlinji'  on  the  mechanical,  side.-"  I  i-liall, 
therefore,  only  emphasize  certain  points. 


I'HODI  <TIVi;  NKIMIIHTIS.       \  ISCKUAI.  CIIANCiKS.      (KI)KMA      H>.') 


'I'lic  oldest   (•()ii('<'i)li()iis.  now  disrardcd  as  (>ss<Mitiid  reasons 
for  the  production  ol  o'dcina  and  liydro|)s,  placed  the  liydra-inic 
condition  of  the  iilood  as  forein<tst  factor.     It  was  tlioiinht  that 
the  liradiial   withdrawal  of  seruiu-alhuinin   was  followed   by   a 
thinnin,ii(»f  the  l)lood,  and  that  this  was  easily  iwrineaMe  throiivih 
blood-vessels.     'Ihis  idea,  however,  is  in  conflict  with  too  main- 
facts  to  !)(•  of  essential  cons<'(|iience.      Later,  the  hydra'inia  was 
a.scrihed  to  water-retention     a  true  liydraMni<'  plethora,     'i'his 
latter  was  particularly  championed  liy  Hartels.  who  especially 
emphasized  the  inverse  relation  of  diuresis,  (edema,  and  hydrops. 
However,  there  are  suHicient  evidences  to  deny  an  es.sential  role 
even  to  a  hydra-mic  plethora,  for  the  reason  that,  as  Senator 
early  pointed  out,  (edema  ap|M'ars  fre(|uently  .so  early  that  the 
existence  of  hydra-mic  plethora  may  he  ruled  out  with  certainty, 
and  that  diminution  in  the  amount  of  urine  does  not  even  lead 
to   a    hydra-mic    plethora.     The   most    distinvinished   objection 
came  here,  ajiain,  from  Cohnheim.  who,  with  Lichtheim,  |)r()- 
duced  exjH'rimentally  in  animals  a  hydra'mic  j)lethora  of  prob- 
ably jireater  dejiree  than  is  ever  preseni   in   the  human   iKMng. 
Such  exjM'riments  were,  however,  rever  followed  by  aiia.sarea. 
But  if,  on  the  other  hand,  irritative  inflammatory  conditions  of 
the   skin    were    pro(luc(>d.    the   (edema    readily    followed.     For 
in.stance,  if  the  femoral  vein  of  a  healthy  doj:  was  tied,  no  oedema 
occurred,  yet  if  now  a  considerable  amount  of  a  sodium  chlorid 
solution  was  infus(Ml,  anasarca  resulttn'.     If.  further,  one  of  the 
hind  paws  of  a  doji  was  irritatcnl  .so  as  to  Un'ome  inflamed,  and 
cannuhe  were  in.serted  in  the  lymph-ve.ssels  of  i    th  lejis,  it  was 
olKserved.  after  injection  of  a  sufficient  quantity  of  a  solution  of 
XaCl  into  the  jufjular  vein,  that  decidedly  more  lymph  dropjx'd 
from  the  inflam(>d  extremity,  while  the  healthy  .side  showed  no 
appreciable  chanjre.     The  .same  occurred  after  the  hydremia 
was  continued  for  several  days.     Cohnheim's  conclusion  was, 


I1H-. 


HKinirr 


DISKASK 


llit'icfnic.  ilirit  iiiiaci  vessels  through  wliirli  a  normal  1)I<i<mI- 
strcaiii  flows  never  jiive  ri,s<'  to  (nh'iiia,  that  the  hitter  is  the 
result  of  a  direct  injury  to.  or  nutritive  disturlianees  in.  the 
vessel-walls.  These  views  found  further  corrol (oration  in  otlier 
observations.  1  may  only  rec.ill  to  your  mind  that  certain  drut's. 
like  arsenic,  of  which  a  tlirect  injury  to  vess<'ls  is  assumed,  lead 
to  the  |)rodu<tion  of  (edema  Maxims,"'  finally,  has  (>xten(led 
the  e.arly  observations  of  Cohnheim  and  Lichtheim,  and  showed 
the  snsce|)til)ility  of  the  l)lo(«l-ve.s,s'ls  to  a  numlu  rof  .substances, 
anioiii;  them  the  retained  normal  urinary  products. 

Of  <ireatest  interest  and  supjMtrt  here  is  also  the  direct 
evidence  furni.shed  by  certain  forms  ((f  nephritis  in  which  we  can 
easily  reco^rnize  marked  injury  to  vessels.  This,  as  you  recall, 
is  particularly  the  ca.se  in  scarlatinal  nephritis.  In  scarlet  fever 
the  blood-ve.s.s(«l.s.  not  only  of  the  kidney  and  throufihout  the 
whole  body,  but  of  the  skin,  are  in  decidedly  irritated  condition, 
and  u'dema  is  one  of  the  most  prominent  .symptoms.  Senator, 
therefore,  extending!  these  views  of  ("ohnheim.  s|)oaks  of  the 
nephritic  hydrops  as  a  "hydrops  irritativu.s."  We  could  easily 
(juote  more  eviden-e.  j)articuliuiy  of  an  exjM«rimental  nature, 
to  support  the  view  that  the  condition  of  the  bkxul-ve.ssels  in 
other  words,  the  toxic  action  of  some  irritant  u|K)n  them,  when^by 
their  jH'rmeability  is  increased  is  of  paramount  importance  in 
the  production  of  nephritic  (edema. "  I  will  desist  from  doinj: 
it  l>ecaus(>  evidence  is  here  so  .stronji  tliat  we  accept  it :  but  the 
(juestion  remains  whether  it  is  the  all-important  and  only  factor 
in  this  matter.  This  possibility  must  1k'  denied.  For,  as  we 
know,  increased  transudation  is  by  no  means  identical  with 
u'dema.  In  order  to  obtain  the  latter  there  must  1k>  added  an 
interference  with  the  lymph-flow.  This,  however.  deiH'nd.s,  as 
you  recall  from  your  physiolojiical  studies,  tipon  the  pressure 
diffe'-ence  in  the  capillary  and  lymphatic  systems.     The  pre.ssure 


PUODl  (TIVK  NKI'HItlTlS. 


VrS(KH.\l.<  HAXdKt*.      (KDKMA     Wl 


ill  tho  IvinphaticH  is  partly  (U'lM-mlcnt  ti|K)n  thr  l.l(M)(l-pro«Hure 
an(J,  as  l^iiulonT '-'  luus  shewn,  the  tissuo  tension  (.f  tlio  surround- 
ing' structures.  Magnus  and  Krohl  "  have  |x.intcd  out  that  thes<> 
may  vcr>-  well  Ik-  involved  in  nephrites.  Biit .  unfortunately,  we 
have  as  yet  no  reUahle  data  alK)Ut  the  tissue  tension  in  nephritis. 
It  seems,  nevertlieless.  very  jKissihle  that  the  sam.'  tc.xi.-  sul.- 
stanees  which  injure  vessels,  injure  tissue  elasticity,  either  di- 
rectly or  l)y  hijrh  osmotic  pressure  with  water  n'tention.  V«>u 
recall  tlu'se  views  as  familiar. 

But  it  seems  that  the  chaiifies  which  take  place  in  the  lym- 
phatic apparatus,  and  with  which  I  made  you  accjuainted  a  few 
moments  a-o.  have  not  received  adcjuate  attention  in  their 
relation  to  the  production  of  mlema.  These  indicate  that  there 
must  also  Ix'  a  decided  interference  with  lymph  resori)tion  and 
lymph  motion,  for  it  can  certainly  not  U"  conceived  how  lym- 
phatics which  display  so  prominently  the  effect  of  irritative 
influence  .)n  the  form  of  productive  and  ol.literative  lymphanjri- 
tis  and  jMMilvmphanjjitis  can  contimie  their  normal  functions: 
and.  as  a  matter  of  fact,  they  would  he  called  uiM.n.  under  the 
previouslv  outlined  conditi(ms,  to  do  increa.sed  (hity. 

I  am  inclim'd.  indeed,  to  regard  the  chanjies  in  lymphatics, 
for  which  vv(>  have  anatomical  foundations,  as  very   essential 
for  the  production  of  any  patholofiical  transudate,  as  not  even 
("ohnheiin  could  produce  (edema  after  injuiy  to  the  vessel-wall 
unless   the   blood    was   hy.lruMnic.     In    nephritis,    however,    it 
fre(iuentlv  oc<-urs  l)ef(,:e  hydra-mia  has  develoi^ed.     The  lym- 
phatics have  usually  been  jiiven  a  very  subordinate  position  in 
the  relation  to  (edema,  mainly  on  the  ground  of  certain  evidence 
which  has  demonstrated  extensive  anastomosis  amonj;  them. 
Obstruction  of  even  lai-e  lymphatic  vess(^ls  is.  therefore,  usually 
not  followed  bv  anv  accumulation  of  lymph  and  production  of 
(iMlema.     But  "tlu^se  facts  are  hardly  applicable  to  the  question 


\m 


HKKiin's    IHSKASK 


of  (i-<lciii.i  ill  iK^pliiilis.  for  thr  iviisoii  lli.it  we  :ir..  not  only 
»l<'.iliii;j  Willi  I  ln.:ili/(..|.  iiic<|iMi>i(:iI.  lyiiiplint ic  iiil<Tfcn'iic(.. 
which  iii;i\  he  :i(l.iiistr.l  l.y  c.iiiiiK.iisatory  Mctinii  of  hciihhy 
lU'idilM.iinu  lymph.ilirs.  I.iit  wiih  ;i  ■irii.'nil  iniliilivc  ••oii(lili.)ii 
wliii-h  involves  mI!  the  tissue  lymphaties. 

If  we  finally  take  into  acfoiint  the  eheiniral  chanties  which 
occur  (liiiin-i  certain  nephrites,  ami  to  which  some  (,f  the  Kreneh 
invest iualors  have  attril.iiled  much  infliience.  we  can  readily  see 
liow  they  may  add  to  the  ease  with  which  l.|oo<l-seriini  |)asses 
through  injured  vess<.|-walls.  If  h:,s  lieen  demonstrated,  for 
instance,  that  retention  of  \a(  1  has  .at  times  coiisiderahle  in- 
fluence on  the  production  of  o'deina:  hut  this  has  U'en  found 
v.irial.le.  inconsi.mt.  .md  therefore  is  in  all  |)rol.al.ility  not  an 
essenti.al.  I,i:i  ;,  contril.ulory.  f.i<tor.  'i"o  the  same  contriKiitoiy 
category  would  Ik'Ioiij:  hydra-mia  and  vemnis  stasis. 

Jo  sum  up:  The  (edema  of  nephritis  depends  primarily  on 
an  (iiitpiit  of  serum  through  injured  capill;iry  districts,  which 
cannot  \h'  removed  on  account  of  similar  injury  to  the  lymphatics 
;ind  prol)al>ly  the  surroundinji  tissues.  |,ater  in  the  di.s,.i,.s« 
metaliolic  .md  mechanical  circulatory  distuihances  as  well  as 
retention  may  alter  the  comi)osition  of  the  hiccd  .-ind  the  vo.sel- 
walls  to  favor  further  the  pa.s.saiic  of  watery  «-lements  thi<iu<th 
the  c;ipillary  system. 

The  term  •'transudate  '  is.  therefore,  not  .strictly  correct  to 
apply  t(.  the  nephritic  (edema,  and  we  may  properly  follow 
S'liator's  precedent  and  speak  of  an  -(edema  and  hydrops 
irritativus."  which  at  once  hrin-is  these  in  the  clo.se  relation  to 
the  exudative  inflammations  of  .serous  memhnmes  with  which, 
as  our  experience  taujiht  us.  they  so  fre(|Uently  complicate  and 
terminate. 

We  liave  traced,  therefore,  nephritis,  increased  Mood-pres- 
sure. hyiMM-trophy  of  the  heart,  anasarca,  hydrops,  and  finally  the 


I'UODI  <   IIV 


NKI'MHITIS.      VIS(  KUM.    (  II  A\<iKs.      tKDKM  A      I'.WI 


frniiiiiiitini:  inH:mim:iti(.iis  of  tlic  si-n.iis  iiu-ml.niiu's  to  a  uniHu- 

rclalinii. 

AikI  ii(»\v  :i  i)ailiii!i  wor.l.  nr.  iHtlcr.  a  sii^ijii'stioii  from  tin- 
I)atli(.l..;:i«al  aiiatninist  I.,  ynii  as  .•rmiciaiis.  (.11  iIm"  syinploiiis  (»f 
..(•phritis  aiul  lli»-ir  ivlati.m  I.,  the  i.rpliriti.-  picccss.     I  .lo  m.t 
inraii  to  liiv  you  l)y  a  dctail.-.l  .lisrussion  of  lli('s<'  symptoms, 
wiiich  must  Ik-  left  K.  soiiu'  n.miH't.'nf  cliniral  .'XiK)silion,  hut 
I  !io|M'  I  havr  impressed  '.ipoii  you  duriii;!  these  lectures  that  110 
ne|>hiili<-  process  is  all  inde|H'ii.leiit   li'si..n  of  the  kiihiey.     For 
it  d<-p«'iids.  in  an  essential  dejin'*'-  >MM.n  concomitant  and  corre- 
lated chan-es  outside  of  the  kidney.      Ihis  is  so  much  the  case 
that   tiiese  ac(|;iire  here  an  iinp<.rtan<-e  alm..st   unparalleled  in 
the  .liseases  of  other  oi-aiis.     We  saw  in  the  study  of  the  anatom- 
i,-al  features  that   we  must   sharply  separate  the  results  of  the 
i„il:,ininatory  .hanjies  in  the  kidney  from  thos.'  which  occur  as 
the  results  introduced  l.y  disturl.aiices  from  outside.    Similarly. 
i„  (he  sympK.matolojiy  of  nephritis  you  will  find  that   the  com- 
plex clinical  lectures  of  the  various  ty|M-s  may  he  separated  into 
two^M-eat  ^roui)s  of  symptoms     the  renal  and  extrarenal.     The 
i„,por1an<-e  of  those  in  iii.lividual  <-ascs,  as  you  -an  iradily  see. 
varies  .-onstaiitly.     In   the  early   staples  of  slowly   projire.s.sinji 
pr(.<luctiv(>  ne|)hrites.  for  instance,  the  extrarenal  symptoms  are 
of  much  fireater  value  and  im|M>rtance  tliaii  the  renal,  for  the 
kidney   is  still  sufficient,  and.  if  anythinjr,  hyiM-rfunctionates. 
N„t   until  much  later  occur  the  suiM-radded  eviden.-es  of  the 
serious  renal  involvement.     Vi<-e  versa  in  some  of  the  rapidly 
tlevelopiiifi  exudative  de-eneralive  ty|H's.  the  symptoms  of  the 
renal  afTection  may  dominate  from  the  start,  and  later  l)ecome 
modified  hy  the  extrarenal  chanjies.     Herein  liesa  jjreat  difficulty 
in  the  studv   of  renal  infiammations.     And   if  this  offers,   as 
I    pointed    out    at     the    hejiinninji    of    these    lectures,    fireat 
ohstaeles  on  the  anatomical  side,   they   are  necessarily  nuich 


L»(M) 


liUMillTS    DISKAsi: 


'^vvMvv  on  the  .lini.al.  \\V  may  fin.l  in  this  aLsf>  tho  cause  for 
tlic  <.<-casionai  c.nflict  l.(«lw,-oii  (ho  views  of  the  patholofrica] 
.•"iMK.inist  aii.l  th(«  cliiiiciaii.  The  hitter  ehissifies  neeessarily 
hiruely  a<r..i(lin-  t..  c.rtaiii  -iroiips  ,,f  syinplc.ius  and  weli- 
eslal.lisli(d  fiiMcliunal  (iisturhaiices.  which  represent  th(>  sum 
'••tal  nf  the  interfereiiees  pnuhiced  l.y  a  (Msease  in  t  lie  relation 
of  all  \  is.rra  to  ,.ach  other.  Thr  former  classifies  the  chanjics 
ill  «'Me  or-an  acconlin-  to  their  pathojicnesis.  and  endeavors"., 
•iiiMlyze  them  m  more  or  less  ahstract  independence. 

Wehavearrive.lat  the  end.  I'erhaps  my  presentation  of  the 
■  ii'.ie<'t  has  scrmed  v<'ry  ..Id-fashioned  t<.  yon.  It  p.-rhaps  has 
i'een  .li.MMisse.l  t.i..  mu.-h  for  y..nr  tastes  i,,  wcll-t,,,,!,!,,,  path.s.  or 
it  h.-is  n..'  ac.|U.aiiile<l  yon  with  new.  startlin-  i.leas.  Hut.  after 
•'"•  ''  '"••':•  '"•  "i;'<  o'K'  or  ..th.'r  part  ..f  the  <li,s.Mi.ssi.,n  has  arou.s,..| 
y..ur  ..wn  thought  .-uhI  n'as..n  to  -o  furth.w  than  what  w.-is  here 
jMv-ente.l.  and  y.,M  may  feel  more  en.-.iura-ed  in  this  effort  if  I 
remin.l  y.ni  .,f  .a  remark  C.ethe  ..n.-e  ma.ie:  ■  M\vs  in  .Icr  Welt 
ist  s.-h..n  ..imual  -.■.l;..-ht  wor.len.  cs  ist  mn-  n.-.thi-  (..s  n.u-h  einmai 
zu  .lenken." 


I 


NOTKS   \M)  Hl.FKHKNCKS 

The  litcnitiirc  on  Hrifiht's  .liscnsr  i>  sa  ciidiiiious,  and  of  latr  years  so 
inii.h,  i)arti<-iilarly  .■xt)crinicnt  ',  •  <„k  has  ace  Miiuilatcd,  that  it  has  Ixrn 
p-rf.'ctlv  itiipossil)lc  to  cvi'ii  nii  ..iioii  :ill  th^'  imix.rtant  coiitrilmtions  to  the 
various  i)lias('s  of  the  suhj.Tt.  Omissions  will,  therefore.  I.e  foun.l  fre<iuent. 
and  much  valuable  material  may  have  escaped  my  notiee.  These  lectur.s 
were  not  int<'nded  as  an  exhaustive  treatise  on  the  s\il)jeet.  hut  to  familiarize 
the  hearer,  and  now  the  read.T.  with  the  fundamental  fa.'ts  and  to  sive  him  a 
i)ase  for  own  thought  and  research.  The  notes  and  references  are.  therefori'. 
no  exhaustive  record  of  the  literature.  I.ut  intended  to  sui)l)ly  to  the  reader, 
■lot  only  eorrol. oration  of  ipiotatiors.  hut  to  oiien  a  particular  field  whicli  he 
inav  wish  to  pursue  further. 

FIHST  LKCTrWK 

i.   .Ktiimedicinra-ci  contractu' ex  veterihus  medicina'  tetral>it>li  sive  <iuati'r- 
nicmis  tertii.     l.unduni  MD.M.l.X. 

Sermo  secundus  et  ex  online  (h'cinuis.     Cap.  xx.     He  hydrope  si.e 
atpia  inter  cutem. 
Senno  tertius  et   ex  online  unideciinus.     Cap.   xvi.     De  n'nuni   m- 

llammatione.  .\-iii 

Avicenna-  aralnnn  medicorum  prineipis.  etc.  VeiK'tiis  MDCMll 
.\pud  .juntas.  Tom  i.  I'en  ii.  Do.'trina  :?.  De  significant ihus 
coloris  urina'. 
2.  Hefon'  Morwuini  similar  ohservalion.s  wiTe  n'conle.l  liy  Monet\is  in  his 
well-known  Se|)ulelaetum  anatomieum.  e<l.  Manfteti,  l.Utfduni  MIK'C. 
I.ih.  iii.  sect.  XX.  ohserv.  xvi.  and  later  i)y  .1.  Lieutaiid,  Historia  ana- 
tomico-me.h<'a.  etc..  K.  Portal.  Paris.  ITtlT.  i.  Portal,  Cours  anat. 
medieale.  SeheiK'k.  Otiaervat.  med.  rar..  lil>.  vii.  Morfrasjni,  De 
sedihiis  et  causis  morliorum  per  anatomem  indapitis.  17()1.  Kpist. 
xxxviii.  xl,  and  xlii.  In  the  l.eKinninsj  of  the  I2d  episth'  the  history  of 
the  knight.  (|uoted  fn.m  Valsalva,  will  he  found  i)articularly  interest- 
iiifl,  not  only  fn.m  the  ])atholo(jieal  standi)oint.  hut  as  a  contribution 
to  the  social  conditions  of  the  times. 

:{.  C„tunii;    De  ischiatle  nervosa  coimn.  ntarius.     Vienna-.  1770.  p.  24. 

•t.  In  Hollo:    Diahetes  mellitus.     Chaiiter  vi.  London.  171IS. 

-y.  Observations  on  Dn.psy.  which  Succeeds  Scarlet  F.-ver.  Transactions 
of  Society  for  the  Impn.vement  of  Medical  and  Chirurni.'al  Kn(jwl- 
ed({e.  vol.  iii. 

JOI 


•_'(  L' 


MHK.irr  S    DISKASK 


ti.    Kiaii.lc:    All  Accmiil  ol  S.iiiic  CIimms.s  finm  l)i>rMsc  in  the  Cniiiix.i-itimi 
■  ii    lliiMKiii    riiiii',    I.diiildii.    1S07.     SciiihiiMoic:     A   Tic.-iiisi'  un   tlic 
\:itllir  uT  (  Jiiiil.  I.oiiilim.  1S2:>.  |):ii;c  ;{1.!. 
7.   r.rialii  :    l!c'|)i)ii~  (.r  M.(lii';il  Casi-^.  i.  ls_>7:   ii.  |s;j|. 

N.  Cav-Mii,!  (II.MTVMli..iis  llliistraliv.Mil-  HcmmI  Disease,  A.-cuiiipanicd  with 
thr  Scnvlidii  ..I  All.iiiniiioii>  I'liiic.  l.y  Dr.  Hrifilit.  Cuv's  Muspital 
l{ipnlt>.  v,,l.  i.  MDCCCWWI.  I  npr.Hllln.  I,,.,-,,  his  rxivncit 
'loriipiimi  ni  I  hr  chiiical  history  .if  th.'  ilis,.as,>  for  those  who  arr  imaMc 
lo  fon-ull  the  oriiiinal  on  pp.  o.S'.l.  :U(t.  and  :!t!  : 

■  ^  ''"I'l-  "I'  ;iii  :"1"1'.  i-'  al'tVctcd  with  scarhitiiia.  or  soi ihrr 

ariiir  chscasc:  or  lia<l  in.hil«c<i  in  tlic  iiitcinpcratc  use  of  ardiMit  spirits 
lor  a  M'rii-  „\  iii,,iilhs  or  years;  h.  is  cxp-.s^d  to  some  casual  cause  or 
hahiliial  -oiirce  of  siipproscd  perspiration:  he  finds  the  secretion  of 
Ills  urine  nieatiy  increased,  or  he  discovers  th.'il  it  is  tinci-e<l  with  hiood; 
or.  without  ha\  iiii-  made  any  sudi  ohservalion.  he  awai<es  in  the  niorn- 
inii-  with  hi-  laceMV,,llen,  or  hi-alllJes  piitly.  or  his  liandscedeinalous. 
It  he  hapi.eii.  ill  this  coiwHiioii,  t<i  fall  under  the  care  of  a  practitioner 
wlio  -uspecls  the  natiife  of  his  disea-e,  it  is  j'onnd  that  already  his 
urine  coiii;iiii.  ,-1  iiot.-ilile  i|uantily  of  all>uniiii.  Mis  pulse  i-  fiiii  and 
hard,   his  skin  dr\  .   he  lias  often   liead;i<'lie.  and  soiiietiines  a  sen.se  ,,f 

''■' '  ""'iiili'  across  the  loins.      I'nder  Ireatinent  more  or  less  active, 

or  sometimes  without  .-iiiy  treatment,  the  more  ohviousand  ilistressinn 
of  these  symptoms  disappear:  the  sweliin-.  whether  casual  or  constant, 
1-  111.  loii-ier  oliserved:   the  urine  ceases  t,.  evince  any  adini.\ture  of  red 

particles:    and.  accordinii  to  tiie  dejjr f  importance  wiiicji  h;is  heeii 

att.ached  to  these  symptoin>.  they  are  "jradually  lost  sijjht  of.  or  are 
ahsnliitely  loi-fiolten.  NeNcrtheless.  from  time  t->  tiliu'  the  couilte- 
ii:iiic(.  hecomev  liloated:  the  skin  is  dry:  headaches  occur  wilii  unusual 
''■'■'|iiiii'>  :  or  the  calls  to  micturition  distiirh  the  night's  repo.se. 
.Mter  a   time,   the   healthy  color  of  the  I'ouiltenallce  fades:    a  sense  of 

weakness  or  pain  in  the  loins  increases:    headaches,  often  ace paiiied 

l>.y  vomitiny:,  add  iireatl>  to  the  sieneral  want  of  c^omfort ;  and  a  s,.n,s(. 
of  Lassitude,  of  weariness,  and  of  depression,  uradualiy  steal  over  the 
I'odily  and  mental  traiiie.      .\iiain  the  assislan.'c  ..f  medicin.^  is  sought. 

If  the  n.almv  of  the  disease  is  sus| ted,  the  urine  is  carefully  tested; 

and  h.und,  in  almost  every  trial,  to  contain  alhiiiiiin,  while  the  (|iiaii- 
tity  of  urea  is  gradually  diniinishin),'.      If,  in  the  attempt  to  fjive  relief 

to  the  oppression  .,f  the  system,  hi 1  is  drawn,  it  is  often  hulTed.or 

the  serum  is  milky  and  opa(|Uc;  ami  nice  analysis  will  frcfiuenlly 
detect,  a  iiivat  delicieiicy  of  all.umiii.  and  sometimes  manifest  indica- 
tions uf  the  presi'lice  of  urea.  If  the  disease  is  not  suspected,  the  liver, 
the  stomach  <ir  the  hrain  divide  the  care  of  the  practitioner,  sometimes 


NOTKr 


AM)  i{i;i-Ki{i;.\i!;s 


•_'(i: 


(Iriiwinti  him  av  \y  altop 

Tilt'  swelling  increases  ami  decreaM 


ItDijetlier  fnini  the  more  ii-.iportalit  seat  ol  ilisease. 


the  iniliil  Kl' 


1  urows  eheerl'ul  or  is 


.1;   tl 


le  secret  loTls  o 


fthekidiiev  or  the  sisiii  are  aiisiiiieiiteil  or  diiiiiii- 


ISlUMl,    so 


iiietiiiies   ill  alternate   ratio,  snnu 


times  without  ai)l)arent  re- 


lation.    .\nain  the  patient    is  restoreil 


to  tolerable  liealtlr  ajcain   he 


luties:    Or  he  is,  i)erhai)s. 


enters  on  his  active  i 

swelliiif;  increases,  the  urine  hecoiiies  sralit.v 


tl 


le  |)o\V( 


t'ortunate;     the 
is  of  life  seem  to 


.1.   tl 


le   llin^ 


(edematous  ant 


1.   in  a  state  of  asphyxia 


or 


una.,  he  siiik>  into  the  urave 


jjlottis  c 
solution 


ir  a  sudden  elTusioii  of  serum  into  the 
if  the  air.  and  iirins;s  on  a  more  sudden  dis- 


rs  the  passaj; 

Should  he.  however,  have  resumed  the  avocations  of 


lie   I.- 
auaiii. 


ilsiiallv   suli,i«'ct    to  coiistan 


t    lecunences  of   his  s\liil)toiiis:   or 


almost  dismissiii';  t 


he  recollection  of  his  ailment,  he  is  s-  ( 


ddelih 


sei/eil  Wl 


th  an  acute  attack  of  iiericarditis.  or  with  a  still  more  acute 
thout  aiiv  renewed  waniiiiK.  deprives 


ittack  of  |)erilonitis.  which,  wi 
tiini.   in  eight    and   forty   hoiir-^.  o 


lanni'r  likewis 
iliserved  to  liecome  mo 


e.  other  perils  await    limi; 


•e  iie(i 


f   hi>   lite.     Should   he  escape   this 

lies   have   been 

di'raiiKed:  his 


us   liea<la( 


(lUeiit;   his  stomach  more  ( 


vision  nil 


listinct:    h 


insi  depraved:    he  is  suddenly  seize 


d  with 


ivulsive  fit.  and  liecomes  lilim 


1.  Me  strufiKh'^  Ihroush  the  attack; 
hut  a-iain  and  asraiii  it  returns:  and  hefore  a  day  or  a  week  has  elapsed, 
worn  out  l.y  convulsions,  or  overwhelmed  hy  coma,  the  painful  liistory 
of  his  disease  is  closed.' 
«».  Christison:  ( )l)servatioiis  on  the  Variety  of  Dropsy  which  Depends  upon 
Diseased  Kidn.'ys.  Kdinlmrsh  Medical  and  Surgical  .loiirnal,  vol. 
xxxii.  IS'iit.     .^lid.  On  C.ranular  Defeneration  of  the  Kidney.  Kilin- 

hui-Mlh.  1N:51»- 

Oshorne:    On   Dropsies  Coiiiiected  with  Supiire.-^sed  Perspiration  and 
CoanulaMe  Trine.  London,  1S38;  and.  On  the  Nature  and  Treatment 
of  Dropsies:    Duhlin  Journal  of  Medical  and  Surjjical  Sciences.  1S:}4. 
(IreKory:   KdinluirMili  Medical  ami  Suifiical  .iournal.  xxxvi,  p.  Ul.l,  and 
xxxvii.  )).  ">l. 

10.   London  Medical  C.a/.ette,  vii,  1S:U. 

IL   Dictionary  of  Tract ica'  Medicine:   under  Dropsy. 

12.   Duhliii  .journal  of  Medical  Sciences.  IS;W.  U\. 

IS.  I'rimiry  Di.seases  and  Their  Treatment.  London,  18:}8. 

IL   Uayer:   Traite  (h's  maladies  des  reins.  Paris,  1S40. 

1,-).  Ti.ssot:    De  riiydroi)sie  causee  par  I'affeeti.m  granuleuse  (hs  reins,  Paris, 

It).  Suhatier:  (  onsiderations  <"t  oh.servations  sur  lliydropsies  .symptomatuiui' 
d'une  lesion  speciahMh's   reins,     .\rehive   MK'ix'Tiil*'  de  ineih-cine.    See. 


JIM 


Hl{|t;in  s    DlSKASK 


17.   IV-ir:     I),,    a   \>rvsrnrr  ,|,.   rMll,u,„i,i,.  dans   luriiic,   cmsid.wc  .•oinmc 

|)li('n(>iii.".|r  It  coinriif  -imic  ilaiis  Ics  iiialailit  >.      Paris.  iSIC). 
1>.   <Mii-st:    Ktat  aHu.l  d.s  roiinaissa.i..s  s,ir  la  i.ialadic  .l.s  rvins  .li'sin,,,-,. 

sous   l.s   .i.-i,..i„i,iati,,Ms   ,lr   inalaair  ,|v    MriKlit ,  alT.rtion   firamilrusr. 

nrpliril.' alliiiiiiiiicii>c.     ( la/.  riKMl.  ,\v  |>aris.  |,s;{ti.  p.   1 1!». 
1!».   M.  Solo,,:     I),.  r,.,||,„n ,r i   Imln.psi..  caus.V  par  uii.'  riahulic  .1,  . 

niii<.      I'ari<.   IS.is. 
■21).    I<,.,-,,u,,,l:    .S-..n.-.ioti,|„r  ,1.-  uriiio.  ,„.  Trait.',  .l.s   alt.'r.-.ti.ms  ,],.  r„ri„,. 

ilaii-  l.>  iiiala.lii  >.  I'ti'.      Paris,   isll. 
1.>1.    In   Ca-p-rV   \V,M|,..M>,.|,rilt.   lis.   :>,'.,.    Id.    IMi-t.      .\n.l.   .\„al.Mtii>,.li..  immI 

rml<n.sk,,p,s,.|„.     I  ■ni..rMi,.lni.,ii,„    z„r     ,.llK.Mn..iii,.|,     un.l     sp..,-i,.ll..„ 

I'atlml.'iii.'.  ls:;s.      I.at.'r:  .M.haii.lluri!:,.,,  zur  I'l.v.sii.l.vui,.  ,„„i  I'atlw.l- 

"ni.'.  .L'tia.   IM'.'. 
•-'-'.    Hi'p.Tl.iriiiiii  t'iir  .\riai..iiii..  iiml  l'liysi.il.i}ri,.,  |s;i7,  n. 
-':;.    I).-  r.-iiilms  in  i,M>rl..,  Ilriuliiii  .l..v:.'ii,.ratis.      Di.ss.Tt.  inane.  Hero!.     |,s;{'( 
121.   Z.ii>,|,nri  lVirrati,,n,H,.M,.,li/in,  Isil ,  i.  p.  ,i7;   ii.  p.  .'20.  a,„|  Ha.ulhuHi 

'III-  i-aliiin.'ll.'n  l';itlii.l.i;;i.'.  ii.  |S17,  p.  ;i(i:j  |V. 
2.'>.    1)(    niorlx.  Hriiilitii.  lalaiiiial.  IMI. 
■2*<.  .I.,|ins,m:      M..li.-.,-Clinuriri,al     'I'laiisaiM  i.ms.     xxix.     xxx.     xxxii.     .\l.s,,. 

Til..  Dis.asi  >  ..f  til,-  Kidney,  anil  L.tIuivs  .m  Uriiilits  Disease. 
27.   M.'.lii-.>-('liirmv;i.';d  ■i"ran-.i.ii.in«.  xxix    p   .i\s 
•2S.   1 1, id..  XXX. 

-'!».   Iliid..  xxx. 

:ill.  Cliarii.'  .\nnal.  n,  i,  |n.".(I. 

••51.    |-reri.l,s:    |)i,.  Mri«l,t's,l,..  Nienn  Krankh.it.  ..ti-.      Mrai.n.M.hwei^r,  |s,-,i 
■^2.    H.i.kitaiisky:    l...|,rliu.li  .l.r  patli.)!oKisel„.ti  Anal.iinie.  ii. 
:!;!.   I  .■i..r    paniiil,yinat..se    Knl/iindiinn.    iv,   p.    2(11.      (Cla.-si..    .^^iMml.l  I..- 
r.a.l  liy  .'Xi-ryliDdx . ' 

:!t.    r)i..    Hin.lesul.stan/    d.r    Nier..    in,    ii,-mu,Uu    un.l    krank.^n    Zu-Ian.l.. 

Mi'riin,  |,s.-,.». 
:r..  ('.)liiih..irns  w..rk  ..n  intla.n.natii.n  i^  to  I,,,  .•.msult..!  in  Ids  \  orl.suiiK.n 

til-r    all^i.ni.in..    I'ath.,l.,fri.';     ..n    the    ki.ln.ys    li..    f„ll„„,.,i    niaiidv 

W.'iticrt's  vi.u-.      iliid. 
;!li.   Traul..-s  vi..ws  ar.^  pr.  ,s,nt..l  in:  IVI.er  .len  Zusainin.nlianf;  \nn  ILtz  nn.l 

Ni.r.iikratdvh.il.ii.     I'.erlin.     jS.-.c,;      Deutsche     Klinik.     IS,",!!,    .{j    :{2: 

.MIsiiineine  ined.  Cenir.d/iituns.  IN")H.  i,:,:    Deutsihe  Klinik.   l,S(i:{.' 
:!-.   Kli-lis:    l.i'lirliui-h  il.r  paili.il.iirisih..  Aiiat.ind...  lS7(i.  i,  |i|. 
oS.   Nephrili-  ini.j  .Ml.utninuri..  M.inn.  iSSl. 
Mil.   Di..  l'atli..l..trie  und  Therapi..  .Nt  Ni.Tcnkrankh.  it.^n.  lMi:{  an.)  Isdl. 

10.  \.Thaii.llun-,ii   .les  (uiurr.-s.s  fiir  innere    Me.jizin.     Krster    (  oiicrcss 

1SS2.  '    ' 

11.  (lily's  ll.i.-piial  Hip.irts.  viii.  1S.".2.  2.1  series. 


NOTKS    AND    KKKKI{KN(KS 


205 


l-J.  A  I'raclirul  Tniitisc  on  Hrinlifs  Disease.  K<liiil)urnli.  1JS71. 

i;!.   Mcilico-Cliirurt^iealTransiictitnis.  Iv,  1S72. 

H.   Volktiiaim's  SaniinliiiiK  kliiiiseluT  Vortriifj.',  1S7I.  :i.'),  and  v.  Zienissen's 

HaniltiiK'li  (ler  spee.  I'athol..  ix.  1,  1S7.'>  and  1S77. 
l.V   Nircliow's  Arehiv,  Ixxiii.  1S7S.     Berliner  kiinisclie  Woeliensclirift.  1880, 

No.  2'.t. 
It).   Dielirinlit'selie  Nierenkrunkheit  voni  i)atliolo(iiseli-anatoniisclien  Staiid- 

jmnkt.     Volkinann's  Saniinluni;  kliniseher  Vortrafje,   IS7!I,  Nos.   102 

and  Hi:}.     (An  exeeedinnlv  important  work.) 
47.   TelxT    die     I'rsaelien    der    Nierenschunipfun}!;.     Deiitselies    .\nliiv    f. 

klinisehe  Medizin.  xxv.  ls7'.t,  p.  ')Sti. 
IS.   Meitra-ie  /ur   Keiintniss  des  Morbus  Hrinlitii,  Ziejrler's  Meitra^ie,  Jena, 

lSS(i.  i. 
t'.».   I.oc.  eit. 

.-,().   Die  Erkrankunjieti  der  Nieren.     In  Notlmagel's  series,  W  len.     A.  Holder. 
.')!.   Virehow's  .\rehiv,  xix,  IStJO. 
.VJ.  .\rchiv  fiir  Ileiiknnde,  1S(')7. 

.■>:;.    llandliiieli  der  patliolofjisehen  Anatornie,  vol.  i.  1S7I). 
.VI.  .lournal  of  I-Aperiinental  Meilieine.  ISDM.  iii. 
."..").   I.elirl)Ueli  der  .speeiellen  patlu)lot?iselien  Anatoniie.  18(»:i  li. 
.")ti.    Loe.  eit.,  \mm'  47. 
.")7.  Loe.  eit.,  page  I'.H)  IT. 
.-)S.  Verhandiiint?enderdeutscli(>n  patholosiseln'ii  (leseliseliaft,  .lahrsjanR  lOOa, 

p.  t)4. 
.V.t.   TelxT  die  entziindlielien  Veranderunpen  der  (Jlonieruii.     Arheiten  aus 

dem  patholonisehen  Institut  zu  Leipzig,  1007,  monofirapli. 
CO.  Studies  in  I'atholoKieal  Anatomy,  Acute  and  Chronic  Hrisilifs  Disease. 

SIX'OND  LKCTIRK 

1  Consult:  Schafer's  Histology.  Rolim  and  Davidoff's  Text-book  of  His- 
toh.tjv,  and  St.ihr's  T.-xt-t.ook  of  Histology.  Also  Lundois  and  Ster- 
ling's IMivsiology.  where  hiatologieal  and  jihysiftlrgical  problems  are 
discuss.'d'.  Als(i  KnTich's  Die  Mrighfs.'he  Xierenkrankheit.  ISol: 
Krehl,  Pathologische  IMiysioloKie;  and  Oswald,  Lehrbuch  der  cheiii- 
ischen  Patliologie  (Harnab.sonderuiig). 

2.  The  Devei<.i)ment  of  the  Malpigliiaii  Hodies  of  the  Ki.lney.  etc..  .lournal 
of  PatholoRV  and  Bacteriology.  1000.  vi.  p.  4.')'.». 

:i  Consult  here  particularly  Starling  on  the  secretion  of  urine  in  Schiifer  s 
Text-book  on  Physiology,  vol.  i.  an.l  Hermann's  Lehrbuch  der 
I'hysiologie.  The  former,  particularly,  gives  a  readable  presenta- 
tion of  the  whole  subject. 

4.   Philosophical  Transactions.     London,  1S42. 


•JOfi 


HKKIIIT  S    DISKVSK 


.').    Ill     llic     Wirlifl-     Aklldrliliscln'     Sit /uilJIslicl-irlitr.       M.illi.      nat.     Klussc, 

llciiimiiii  ill  hil.  :iii  ( is.Vt  .  p.  :)l".t;   IM.  I.'.  ( l.^iil  i,  p.  :ii7. 
f.   I.iiduiii.  iliid..  l{,|.  IS,  ij  ( is,s:{i. 
c.    l.inlwi;;.  Wamici's  llaiiilucitcrliiiili.  jj.  (i:!7. 
»;.    Rilihcit:    \inlimv'>    vichiv.   |{,|.  xciii.    Hill.      After  iviiioval  <>i  the  iciial 
iiii'iIiiIIm   ill   lal.liils    IMiImii   oIiscivimI  a   very  aluiiulaiil   Hcivtii.ii  of 
thill  iiiiiic.     Tlirs-  i\|HTiiii<.|its  aic  npcii  to  ulijiM'tioii.  as  Miink  ami 
Senator  point  out.      I.oc.    ,ii..  p.  j:;.  foot-note:    and.   further,    Uoyd, 
.hiiirnal  of  I'hysio|oy,y,  vol,  wviii.   l".tlL>.     The  later  evidence:    Mans 

Meyer,     leliir    Dilirese.      Sit  zuiinslieriehte   d.    (  Hsellsehaft    >.lir    Mefor- 
deriinfi  der  jiesanmiten    NatiirwisMiisihafleii.      .\I;irliiiru.  IlKfJ.  p.  !f_> 
i\'.     <  iishny.  .journal  of    I'liysiolotry.   I!ML>,  vol.   wvii. 
7.  Cited  .ift-r  Starlinn.  .Mecliani>iii  of  the  .Secretion  of  Irine,  in  Scliafer's 

'l"e\I-lM,okof  j>liy>ioloiiy.  vol.  i.       I'lVlfer,  <  )siiiot  Isclie  riiter~i|c|ninKell, 

Leipziii.    |s77,      Dreser,    .\irhiv    fin-   e\pcri ntelle    i'atholoijie    iind 

Piiarinakolonie,  l.sit:.',  \\i\,  ;{()7. 
S.   \'erhaiidlini!;eii   der   Deiitschen   patholoiiisi'licn   ( lesellscli;ift.     .I.ahrttanj; 

I'.IO.-..      .Morliiis  Mrinhtii.  p.  (14  tT. 
'.I    ".r:-lauer  ar/tliche  Zeitsclirift,  lS7!t.  22.  and  extensive  discussion  in  ller- 

nianiis  Haildlpuch  der  IMiysioloyiie.  v.  i.  pp.  ;{(!<». 
1(1.  Oertel:  'I'heories  of  Iriiiaiy  .Secretion  from  the  Patholos-icaj  Standpoint. 

New  ^■ork   I'niversity   Mlllletin  of  the  .Medical  Sciences,  vol,  ii.   No    •> 

April.  I'.HL', 

11.  Soliieranski:    Archiv  fiir  exp.  Path.  ii.  I'liarm..  xxxv.  111. 

12.  Senator:    Die  .Mlmmimirie.   IS,S2.  uives  a  full  discussion  of  this  subject 

ami   further  references.      .VIso.    X.Tliaiidluniieii   der   Herliner    Physiol. 

Cesellschaft.   Dec,   IC.   |S,SI.  i,,  Dll  Mois    lieyinomrs   .\rcliiv.   l.SSl.  and 

Mcrliiier  klin.  Wochenschrift.  ISN,'). 
1:5.   Munk  an<l  Senator:  Ziir  Kennini.ss  der  Xierenfuiiktion.  etc..   Nirchow's 

Archiv.    114.    p.    I,    l,s.ss.     Senator.    Teher   Transudation.    \ircho\v's 

Archiv,  III.  S.  2i;t. 
I  1.   Fr.  .Miiller:    I.oi-.  cit. 
1.").    I.oc.  cit. 

Hi.   .Vrchiv  fiir  experimeiitell.'  I'atholr.rie  mid  I*harmakolu}jie,  vols,  xlviii  and  I. 
17.  (iottliel)  und  Magnus:    Il>id..  vol.  4.">. 
IS.  Hofineister's  licit riisre.  ii.  l!t()2. 
lit.    Iliid..  ii.  1!I(I2, 

2(1.   Teller  Diahetes  insipidus  und  andere  I'olyurien.     Deiitsches  Archiv  fiir 
kliiiische  .Medizin.  IlKC).  vol.  S:{.  p.  (17  IT.     ((Quotes  the  other  literature) 

21.  .Vshcr.  Tropp  and  .Michaiid:   Zeitsclirift  fiir  Hiolojiie,  Md.  }.-,  n.  4(j. 

22.  1,0c.  cii. 

2:{.  Zeitsi'hrift  fiir  klinisdie  .Medizin.  :j:{,  i,  1S!»7;  :{4,  i.  ISK.S. 


NoTKs  AM)  hi;ki:i{i;\(i;s 


•2(1 


Tinm)  iKcnHK 


•ilirili"  mill  iillini  .yiil'irvls 


(!i  iicrnl  ri )( I'l  nil   ifirl:.'*  mi  iiif), 
Senator:     Die    Krkrankiiniiiii    ilrr    Nicrcii.     Wicii.    V.Wl.     AlfnMl    Huldcr. 

((iiioirs  literature  extensively.     Very  \x.uin\  liistorieal  inlrodiietion.) 
Kaut'iiianii;    Lehrliucli  der  specielleii   patlioloniselien  Ariatoinie,  Berlin.  I".M)7. 

(ieiru  Keinier.     (Kxci'Uent  tor  rel'erenee  ami  literature.) 
Ziejiler:    .Mlsenieine  i'.itlioiotjie  und  patliolosiische  AnaloiTiie,  Hand  "_'.  Jena. 

l<M»r>,     Hiistav   Kischer.     (Literature.) 
Cohidieiiu;    Vorlesunfieii  iii.er  all}ienieine  I'atlioioKie,  Merlin,  |SS(».     Antiust 

Hirseliwald,  Zweiter  Hand. 
Krelii:     ratliolottische   I'liysiolojiie.    I.ei|t/.i(j.  Iit(l7.     ."itli   Aullasie.      1".   < '.   \V. 

Vomel.     irartieularly  for  llie  functional  eliantje>. ) 
Ortli;   Kelirhueli  der  speciellen  patliolojjisclien  Anatoniii',  U.  Hand.  I.  Ahtei- 

lunti.  Merlin.  IS!«.     A.  Hirseliwald.     (Literature.) 
Freriehs:   Die  Mri({lit'silie  Nieren  Kranklii'it.     Hraunscliwein.     Vieweu,  1S,")L 

I  With  review  of  early  literature. ) 
AseliotT:    Lelirl>ueli  der  i)atiiol()M;isclien  Anatoniie,   IL   Md.      Jena,   Fiselier, 

1  <)(•!). 
Iloelie  et  Hri(iuel:    Les  Lesions  dn  Hein,  Paris,  1904.     (With  tjood  atlas.') 


S. 

!t. 
10. 
11 
12 

i:{ 
14 
IT) 
li°) 
17 


Morl.us   Mritihtii.      VerliantllunKfn  der  deutsclien  patliolofjisehen  tJesell- 
s<'liaft.     Jalirnang     I'.tO.").     p.    ti.").     Naturforselier    VersaininlunK    in 

Meraii,  100."). 
Die    VerandenintJfn  der   inenselilielien    Niere   nacli    Sul.liniat versiftimn. 

etc,,  Zienltr's  Heitrase,  vol.  xlv,  p.  U«. 
ll.id.,  p.  241. 
Il.id.,  p.  2(M). 

Cellular  l'atliolo)j;ie,  lierlin,  4.  AwH..  1K71. 

Die  Lelire  von  der  triihen  Seliwellunfj.  Preis.selirifi,  \inzl.iM-K,  ISOl. 
Virehow's  .Vifliiv,  .'xlix,  p.  4t)l. 
Kleniente  der  PatlioloK"'.  '■'>■  AuH..  1S0(). 
VorlesuiiKen  iiher  allneini'ine  Patliolosji''.  1^><-- 
Allnenieine  I'atlioloRie,  ISSO. 
Lelirl)ueli  cler  allfjenieinen  PatlioloRie. 
Lelirhueli  der  alltjenieinen  patholoniselien  .\natoinie. 
Lehrbucli  tier  iiatholotjisclien  Anatoniie. 
Haiulliueh  der  allnfineineii  Pathologie. 
Virehow's  Archiv,  cxxxv,  p.  470. 

Teller  triilie  Seliwellunn,  Zienh-r's  HeitriiRe,  xxxiii,  VM\. 
Internationale  Zeitsehrift  fi'ir  Anatoniie  und  Phy-^iolonie,  189.'). 


•JOS 


HliKIMT  >    Disi:  \si-; 


IS.    \  itIimIIiIIiIIIUcii   iIiT  iIiIIImIkii    |);illliil(icis(lii'n   (  Icsi'llschuft.    l".l(l((. 

lit.  1,(.,-.  .11, 

•JO.  The  l'liiui|>liM.r  l':illi<il.iii.v,  vol,  i.  I'.HIS. 

•21,   I.fhiliiicli  cl.  spccji'llcri  patliuKi^jisi'hi'ii  .ViiMtoiiiii',  ii. 

22.  ."^iicriflli'  |i;itliiiliiu;iM'hc  .Uiiitnmic. 

'2.>.    hcrr;     l.iir,  cil. 

21,    l)ii'    I'liiiilii '.s<'lic'    Nitn'iiUiMiikhi'il.      NdlkiiiMim's    Siimiiiliiii^    kliiiiscticr 

\(irli:iiit'.  lt.2   H.;!,      isTs  7!i.  pp.   Ill, 
2.").   .\r('lu\io  pir  li'  .s/ituzc  incilichc,  |SS;{.  vi.  :{.    Sulla  hypcrlrdtia  coinpcn.-ia 

liiria  ili'i  iriii:  and   Nriil<ii'iiia/i<irii' (IrH'cpili'lin  <li'i  cuiialiriili  oriiiifrri 

(lilla  nialatia  .li  Urij;lil.     llii.l.,  IsM.viii. 
'2ti,   Thiiiil:     riiiir    i>pib.lir    uii.l   I's.'U.ldr.'HctnTatioii   Kci    Nicrciiiiifarktcii. 

\  ii.  h.iw's  .\r.iiiv,  1  IC),  IMMi, 

H.is,-,!.':     Siiinmn.'ii    .l.T    K.ijcii.Tatiiiii    v.in     N'icnti.'pitlii'Iicn.      \  ir- 

.■h.iw's  .\nliiv.  I7(t,  l'.K)2, 

.latia:   Sulla  n«iii.'i;uii)iic  ilcircpilcliii  .l.'l  r.iii'.     .\rcliiviii  per  s.'U'iizc 

nicliili.'.  wiii.  p.  U2o. 

I'.ia:    I'llicr  Nitiiiiirilaik!.'.  Zicjil.i's  Mcitraijc,  ISSH,  v. 
2".  K.'itiau;.'  zur  .Xnatoiiiic  .1.  s  niiliari'ii  Tulicrki'ls.      II,  r.'hcr  Nicrciituhcr- 

kulisc,     \ir.li.iws  .\rchiv.  ISSI.SH. 
2S.   li'li.i-  TuImt'  .■!  uii.l  TulxTkulosc.  Zcits.'lirift  fiir  kliiiischc  Mcdizin,  ix-x. 
•2!t.  Ocrt.i.  II.ir>i.   On  i^pitli.'lial  rnilifi'iati.ni  and  tln'  l".)rinati()n  of  Kpitlic- 

lial  ( iiant-.-.lls  in    Ni'pliri1i>.     I'ulili.'ations  of  the   l{u:;s('ll  Sape   In- 
stitute .il'  ratli.i|.iy:.\ .  (il.v  ll.ispital,  New  York,  i.     (I-itrratun'. ) 
:i(l,    I..).',  .it. 

:{|.   Mcitiaj;.'  zur  K.imtnis.s  .Ics  Morhus  Bri){litii.  Zicslt'r'.s  Hcitrajif,  i,  18S0. 
o2.    |)i.'  .\(tiiiliini.'    uud    ( Icncsf   ilcr  akutcn    Nephritis.     Zie(jler's  Heitriigr, 

n1.  IS!  12. 
:{;{.    Teller  Nepliritis  siariatitiosa.      Fortsehritt  .ler  Me.lizin,  i,   1SS3. 
.•54.   Nephritis  uini  ,\lliuniiinirie,  Honn.  ISSl. 
O.I.    l,ii.'.  fit . 
;!(i,    l,.ic,  cit. 
:!7.   IntlaTnniatiirv  Chaniies  in  the  Kidney,  etc.  .lournal  of    I'atholoKy  and 

Ha.teriolody.  .luly.  I'.ttll, 
;{S,   Zeit.sihril't  fiir  rationelle  Medi/in,  Heft  i.  p.  (12.     .Mso  dcscrihed  l)y  Niusse 

in  Schmidt's  .lahrhiiclier.  ISlIi,  )).  ;<•")(').     Further,  early  contrilmtions 

iiy  Simon.  Meitrajie  fiir   phy.iiol.  uiid   pathol.  Chemie,  i,  p.  1();{,  and 

Scherer.    ( 'hemische    und    mikroskopi.sclie     I'litersuchuiinen,   Heidel- 

li.'rc.  INJ;?. 
:19.  Hovi.la.  in  Mole.sehott's  rnt(T.-U(hunn<'ii  zur  Naturlehre.  1872,  xl,  1. 
40.  .\rchiv  fiir  experimentelle  Pathologie  und  l'hariiiakoloj;ie,  vi,  p.  113. 
11.   1,0c.  cit.  and  Die  nonnale  und  patlutlopische  Anatomic  und  Fhysiologio 


NOTKS    ANO    HKKKKKNTKS 


2()9 


42. 

u. 

4,"). 
4{i. 

47. 

4S, 


4!t. 


51 


.l.-r  Nior...     Hit.li.,tlu..a  .nr.li.u  C  H.  un.l  Hil.iunK  <kr  hyaline.  Zy- 
lin.lcr.     ('fntnill.latt  f.  allu-  I'utl...  iv,  lH«):i. 

Loc.  cit.  ...  •••    iivi 

r,.l«T  tri.hc  Schw.-UunR,  in  ZioRlor's  HoilniRf,  xxxin,  l.M. 
(irunulahil.lunK  L.m  Nirrrn.-nt/u.ulunK,  ZL'^Lt's  B.-itriiK.N  vn,  M.ppU- 

incnt,  I'.K)"). 
Isnicl:   VinlK.vvs  Archiv,  cxxiii.  ... 

Krn.t:    Fil.rin  in  hyulin.-n  Zylin.iem;   Zieglcr  s  HntraKC  xi",  18)3. 
Xatur  un.l  Kntst.-l.ung.l.T  Nim-n  Zylin.l.T,  <  Vntrall.iatt  fur  allR.  Pathol.. 

iv,  1S'.«. 

z'iiift  fur  kliuisd...  M.-.lizin.  i,  1871..     CentraU-latt  fur  .lie  nu^z. 
Wissons,.l.aft.-n,    1HS().     Singor:    Zcitschrift   tur  Hcilkund.-,   vi.  IHHo. 
Colmhi'ini  also  hcltl  to  tliis  possilnlity. 
Vircliow's  .\rchiv,  Ixxvi.  „„i.,*„,i 

I'usu.T  (VinlM.w's  .\rrluv.  Ixxix)  looks  upon  nu.st  rasts  as  coagulate 
■       ,ransu,l...l  or  .-xua.-l  all.un.in,  and  .l.Tivs  th.  .■oaculatuiR  fmnont 
from  tl...  .lisint-'sration  of  tl...  U-.ik...'yt.-s.     Similar  wTr  Ur.Rorts 
views  (Vircliows  Arch.,  Ixxii,  p.  2.")4i. 
Loc.  cit.,  .lournal  of  K.xp.  Medicine.  , 

;  r..l„.r   Kctt infiltration   un.l   fettige   DeRcneration  d.    N.ercn.  \  irehow  s 

Archiv.  ISO.  HH).'). 


For  urn  lkctuhe 

1  Tlu.  observations  of  I'etrone  (1881)  and  l'is.-nti  (1884)  on  the  „c-w  f..rma- 
tion  of  glomeruli  an.i  new  tul.ules  have  uen.-rally  he.-n  rejecte.l  l.> 
later  investigators. 

2.  Loc.  cit.,  p.  !••.». 

4:  Zur'  Entwicklungsgeschichte  des  Krel.ses  nehst  Henu-rkunRen  iiher 
Fettl.iUlunR  in,  thierisehen  Korper  und  patholoRische  Resorption. 
Virehow's  An     v,  i,  p.  94,  1847. 

5.  I'ettenkof..r  an<l  Vo.t.  in  LiehiRS  Annalen,  Supp.  u,  .161,  ^''^schnf  fur 
HioU.Rie,    vi,    277    (1870);    vii,   4:«    (1871).     Bauer:     Ze.t.schr.ft    f. 

Bioloeie,  vii.  ^^„        ,      .     .  • 

Die   EntstehunR  von    Fett    aus    Eiweiss,    etc.      PfluRer  s  Archu,    .-, 

18*)9 
C.iht'es  eine  fettiRe  DeRencration?    VerhandlunRen  des  l.^ten  KonRresses 

fur  innere  Medizin,  1897.     And,  Ueber  Fettwanderung  Verhandlungen 

des  13te  KonRresses  f.  inn.  Med.,  189.1. 
Ueber  Fettgehalt  des  Blutes  u.  einiRer  OrRane  des  Menschen,  \  ircho^  s 

Archiv,  174,  1903. 


0. 


•_>lu 


HUK.in    >    nisKASK 


'.».    I(l..i     |Vtl.ni~:il/    nil     l'liirrkoi|H  r.    M.il.    /,.  nli;ill'l:ill .    s.   IW-'.      Ali.l, 

IMIiimi-  Aivlnv.  :!l.  II,  l>vi. 
III.  I!,i\.  M:m  D.iiiioll  :iiiil  l.il-k.  Aiiiilir;iri  .lipiirn;il  nl  l'li\ -iuluuy ,  IS'.I'.I. 
ill.  I.ii-k  .iiiil  MMiiiltl.  i.Milic  .\t\i\  in  lnlriinti|i:ii\  M(t:ilH.liMn. 
il>l>l..  I'.HMi,  \vi.  I.ii-k.  M(i;il»ili»Mi  in  IMiu-.pliiiin«-|'"i-'">'i'^i  '''"'•• 
I'.MIT.  \i\.  I.ii-k.  riic  i;irniinl-  ill  III''  >rnni<'  nl'  Niiiiiliiin,  I'.MM'i. 
SmuihIi  r-. 
II.    I  rlicr  iA|»riininlrll  n/riliili'  |Vll-\  mlii-r.  111-.,   \  iiiliiiw-  .\ii'liiv.   171. 

I  ".mi:;. 
r_'.   {.ill  Tiinirc  «in  :iiiiip|.\-i-i:    Cinlur,   Dii'   l\lini>i;li-|i:'*liiiliim-rlii'  Mcdnituint 
iliT    \iiliil.\~r.   Mnlinir  klini-ilif  U  uclii  n-ciirili ,   I'.Hi:!.  \i,   IV").     Ojiic, 
.IuiiiiimI  111'  1a|i.  .Mill..   I'.Mi'i.  vii.  p.  :!lli.  T.Vt.      IIimhi'.  Nntc  mi  Aii- 

liii>>i>   in    l.uli.ir  Mini    I  nn-ihiil    l'niiiniiini;i.     'ri;ni-Miliiins  of  As- 
>(iri:ilinii    111    Ainiiii;in     l'li\ -iriMii-.     mdo.    wiii.     W>"i'i.      \V:ililvii«i'l, 

.\nliii\-r   iHiii   Irltiiii'    Diiiini'ialiiiii.    Nnrlmw'-   .\iiliiv.    I'.lltl,    I".'),   i. 

l'liii~pliiir\iTiiilliiim  nil. I  Aiiiul\-r,  DmNi-ln-  .Vnliiv  I',  klin.  .Mnli/.in. 

I'.iii.'..  vj.   t:i7.     I'.  .Miillir.  I':iiliiilii!iir  ili-  Sintlwiili-iU.     Lcvrni',  I*. 

.\.:    .\nliily-i-.  IImimv  l.niiins,  N.  V.,   llHI.'i    llMMi.  I.ippinnitl  Co. 
|:{.   .\n  iMilliiii    l)i-iMi-.>.iiin  in  .Viliinii"- :iililiv~- luroif  the  Niw  \i.rk  lliirvoy 

Soiiii>   nil   M,vilin~.  ill..  pulili>linl  in  till'  Ihiivi'V  l.ii'liiir>  lor  IllOtl 

to  I'.III?.  Niw   \iiik.  I.ippiniiitl  (n.       For  iIh'  ■liiini-lry  -ir  ll;tnmirr- 

-Ii'ii.   I'liy>ii>li>i;i-rlii'  ('lirinir.   Ii:in-l:iliil   into   I'.nuJi-li  Ky  .1.   Maiiiicl. 

.Vi-o.     lloppi-Srylrr'-      l'li\ -ii  ili  ini-i'll      lllnl      p;il  lioloni-rh      i-jicniisclic 

.Vnaly-r.      A~holV.  Ziiiilrr-  Hiilriii;i\  IM.  17.  i.  p.  7.  iiWf<  tiic  most 

rri-fiit  Mii'l  i\li'n-i\r  ili-i-u~-ioii. 

II.  Orrii'l;    JJiiir.iijr  /ur   l\iniilni--~  ihr  .Xiis^rliiiiluiiiJ  il's  or«;aniscli«t'liuinl- 

iii'ii  I'lio-piiDi-  iiii  llani.  Ziiisi-lirilt  I'.  pliy>iol.  (  limiii'.  xwl.      Keller. 
iliiij..  \\i\.      M.illliiMiii.  jiioiiiiinii'ai  .loiinial.  iv.  '>.  li.  ami  7.      Maiiiiel 
.mil   Oirlri.  N.  \'.  r  iivrr~ii\    Uiilliiiii  of   Meiiial  Siiiini-^.  i.  p.  111.'). 
I '.Mil. 
l.-|.   S\ 11-:    .loiinial  of  I'alliolouy  ami  Uarltriolocy .  vol.  \.  I'.HI').  p.  I.'i<    T. 

anil  p.  127  If. 

III.  Sit  ll.'innnerNlrii,   i.ihll>iiili  ilrr  pliy-ioloiji-rlien  (  'llilllir.    I'.itl7.  |>.  '.VAX. 
17.   rii.ir  l'"eninllliraiioii.  .ii-..  Ninliow-  Anliiv.  IMI.  I'.ill.'..      .\l-o.  Order, 

leliir  ila-  .\iifl  iiiiii  \  on  .Myrlin  in  Zellen.  ete..  \  iirlmu-  Anliiv,  1117, 

I'.iilJ. 
IS.    See  Sloerik.  lilier  I'rolaiion  Uml  illierilie  i;io>se  wei--i    Niere.      Sitzmifis- 

lieriilile    ilir    I\.  Akaileiiiie    iler   Wissenseliaflen.    \Iatli.-n;il.    Klas.se, 

Willi.     II,".      IVlil.      isaufniaii.     Sperielle     pal  liolotii>rhe     .\na1omie, 

I'.in7.  |>|>.  7s7  7^^. 
!'.».  S,-  Kraiis.  I'lii  r  I'lliilei;  inralioii  mi  I  Kelliiitill  r.ition.  \erlianillun«i'n 


NUTK.S    AM)    IIIKKIIKVI  KS 


!ll 


,lrr    IVutsclnn   |.atholnt:isrl,.n   ( irsrllsrhaft ,  ^r.'listr   TaKUim.  I'.HU.  p. 

•_>(».  On  tt.r  l.art!c  Wl.it.'  or  Soapy  Ki.ln.y.     .I.mn.al  «{    Mr.li.al    K.s.-arrli. 
Hn-iiiii,  XX.  p   27. 

21.  I.'"'.  Ill- 

22.  I.«"'.  'it.  . 

2;{.   I'.'lHr  .1(  u  L.Mill.iiiiJ.'lialt  .l.s  ll.rz.i.s  ii.  .Irr  Ni.t.m.  n.-.,  .\r.t..  i.  rx|.. 

I'allKilc.uic  iiikI  I'haniiak.ili.uir.  .V2.  ITS.  P.Mt.'). 
21.    l.rl,il.il.l.  .1.  .•lu'inisrhr   l'alliol..«ir.    I'.KtT.       lias    a    r.vi.w  of    tl.r    s.ll. 

jicl  (.1'  lal  ili'Kfiirratioii  aiul  lal  iiitiltratioii. 
•>:,    Wi.lni.an:    Di.-   .\invl..i.lcrkrai.kimn.     H.itrau.'   vui,   Zi-^l.T.   xin.    lWt:i; 

aii.l   Maillanil.  in   M.'ili.'al  an.l  Suiunal   Hrpnils  uf  NfW   N -rk  (  ity 

Hospital  lor  Utos.     ||.i.t..r.  ( '.•ntralMalt  iTir  I'atl.oloKir.  M.  xix.  2:i. 

p.  IM'I- 

2(1.  ll.rxh.iinrr;  Hyalinr  Dr^rnrralion  .1.  r  ( linn.rnili  .l.r  Ni.'tv.  /h^uLt  s 
H,.itra«c..  IM.  1.-..  llMl-.t.  ,    „     .    ,  I 

27.  llistolojjy  of  l.ivr  Tissur  Hrpii.rati.ui.  .loi.rnal  ol  lalliolony  and 
Uarlcriolotiv.  xiii.  p.  127. 

2S.   V.rlian.llunurn  .Irr  .l.Mitsria'l.  patliolouis.lan  ( l.s.ils.hait.  I'.MI...      I  HMr 

Morliiis  Mrinlitii. 
•'.,    I|,.rxlaini.r   an.l    Hall:    ICl-r  .li.'    Knlkai.s.lunn  .l.r    Ni.tv.    \  inlu.w  s 

\r.liiv    I7!».  I'.Hl.V  .li.s.uss  this  inall.T  iully  an.l  also  nivc  \\\>-  litrratiitv. 
:«).   r,.|,..r.l.n  .V.is^anu  .l.r  .•yan..tis.li.n  lii.lnralion  .I.t  Ni.'ir  m  Cranulai- 

atro|)lii''-     \Vi<'sl)a.li'n.  \>^'M- 

I'llTH   l-KcrrHK 

1.   Vr.  .Mull.r:    I.o.-.  cil..  p.  '•«»• 

•'    Kaufmann:    I-.'lirl)ii.'li  .l.T  patliolosis.li.n  .Viiatoini.'. 

"{.  Z.ir   K.^nntniss  .I.t  Cir.'ulati.mstorimK.'n  in  .l.^n   Ni.'ivn  !>.■.  (•Iir..nis.ii.r 

int.Tsliti.'ii.T  N.'pl.ritis,  Vircl..)wV  .\rcliiv.  H.l.  71.  |).  12. 
4.   r.-l.rr  .li.'  pui.ktfonuiurn    Kalkk..rp.nh..i..  .•!.•.,  \if.hoWs   .Vivlnv,    M.l. 

n  ■ri...'lii.'rat,'nr  on  arfrioschrosis  is  vry  ..xt.-nsivc.  Tlu'  rolL-winn  will 
1,.,  ,„un.l  us,fMl  for  n.f.n.n..-.  .lor.'s,  Wrscn  t.n.l  Ki.twa-klunK  .I.t 
\rt..ri..skl,.r.,s...  Wi.sha.K'...  UKU:  Maivl.an.l.  r.'h.T  Art.Tioskl.Tos... 
K..nKr..ss  fur  inn.^tv  M.^-lizi...  I..'ip/i«.  1!'<»1.  -^  soin..what  .lill.-tvnt 
.tan.l  is  lak.M.  l.v  -V-laini;  s.r  his  pai-.'r  in  th.'  ( ).'tol..r  nunilxT  ..i  th.. 
AnuTi.an  .l..urnal  of  th.^  M.MJi.'al  S,.i...K..s.  V.WX  "Th..  Natntv  ot  th.- 
\rt('ri<)scl.'r..ti.'  Trocss,"  which  also  covers  Kh.tz's  w..rk. 

,i  loc  .-it  an.l  r.-lMT  -lie  Art.TioskhTosc  .I.t  kl.'in.-n  ( )r«anart.TM.>i.  nn.l 
'  ihn- H.'zichun«.-n /.ur  N.'l.hritis.  Vin-how-s  .\r.'hiv.  17S.  Hyp.Ttrophu- 
nn.l  .Vit.Tioskl.Tosc  .Ut  NiiTcnart.Ticn.  il.i.l..  ISl. 


HHHillT  S    |)|SK\SK 


.?  1 


7.  I'ryiii;  l.lxr  An-  \  .•ruii.l.nmK.'i.  .l.r  arl.ri.ll.i.  ( irfiissr  l.ri  iiiliT^tili.'ll.T 

Ntpliritis,  MnliowV  Ar.-liiv,  M<1.  177. 
s.   IrlMT  .l.n.nisclir   NrphritiH  iiikI    ilirr    IW/.iclninK  zur   Arliri.mkliToso. 

Vjn  liiiw-  Ariliiv.  M<l.  l'.'"". 
<».    ri...iiias  vi.'ws  ii.av  l.r  l-uiwl  ill  Vir.licsv  s  Archiv.  H.l.  lU,  !•:.,  1U»,  lO."), 

KHi.     Also,  lilxr  Mhili-  NiraiiilcriiiiKtti  .Irs  mcnN.lilicliiii    K<.r|MTs, 

Lfi|i/iK.  ISM. 

10.  ICIht  .lir   Vrraii.lrnint:.'!!    klcin.T  Ccfassr  l.ri    Mnrl.iis   Mrinhtii,  .•(<-., 

Niriliiiw's  .Vrrliiv.  Hil.  71. 

11.  r.lMT  dii'  V.r.iiKlrniMKt.n  (I.T  kirin.M  Art.Ti.-ii  Ix'i  Ni.r.'iurkrankiinK.'ii, 

\  inliuw>  Ar.liiv.  l.V.I,  l'.HK».     An.l.  rrpiy  t(.  .Ions,  Vircli-'W  s  Arcliiv, 
M    isd. 
1_'.   r.l..r  Siliniiiipl'ni.Tr  cliiic  Artcri.»kl«Tnsc.     \irclinwV  Arcli.,  IHO. 

i:{.   !."«■.  lit. 

11.   Km/  ilrhcr  l.tlMTrirrlKisr.     Wi.iiir  kliiiisrlif  \V.Hli<'iisi'liritt.  2.  I'.MH).) 

.>iiinlarl\.  has  >li<>\v!i  an  .•iilinlv  cliaiinnl  rcunicraliv.'  r. nstruftiim 

ill  till'  aii'liiit'tiirr  of  the  liver  in  cirrlio.scs. 
l.V  Consult    h.r.'    thr    presentation    of    Krehl,    l'atliolo(jisclie    I'livsiolojjie. 

!,eip/i«.    11MI7.    pp.    M    IT.     (Literature.        An<l.    Senator.    Hie     Kr- 

kraiikunneii  dir  Niereii.  p.  11(1  IT. 
If..   Xinliow's  .Vicliiv.  ixxiii.  Is7s. 
17.  Senator  still  holds  thes.'  views  on  the  uroini.l  of  eliiiical  evi.lence.  which 

he  eon-i.ler>  here  sironner  and  more  eonrliisive  than  the  anatomical. 
l,s.   Teller  .hn   /iisammenhaiin   v..ii    Ilerz    mid    Niereiikrankheiten.    iierlin, 

1S.-.C..     .\nd.   Naehtraiiliche   I5einerkuii«en  da/u  ill    i)euls<'lie   Klinik. 

1S.V.>.    M    and    :VJ.     An    excellent    modern  presentation  of  the  whole 

suhject    of    l.iood-pressiire    ill    T.    < '.  .lanewav's    monodniph.    "The 

Clinical  Study  of  hlood-pn -sure." 
111.  Cohnheim;  Alltiemeine  Tatliolonie.  vol.  ii.  •-Me  Anfl..  pp.  2.-)S  and  M)] . 

•2(1.   Loc.  cit..  ntOJ.  p.  122. 

21.  Patholouische  i'hysiolonie.  p.  :{S.  etc. 

22.  \'erhan<llun)ien   der    Deiitseheii    patholonischen  <  ;escllsrhiift.  VM)->.     (In 

the  general  discussion  on  Hrinht's  disease.) 
2:5    l)u  Hois  l{eviiiond"s  Archiv.  1S77. 
24.  llirsch  and' Heck;  Archiv  f.   kliiiisch.'  .\le(li/in.  C.'.t,  .".(W.  and  72.  o()0. 

Archiv  fur  experimentell<-  Pathol.,  etc..  .-)4.      (.Cited  l.y   Krehl.) 
2.').  I-<ic.  cit..  p.  12.").     Virchow's  Archiv.  Ixxiii.  1S7S. 
2(K   Kxperinienteller  Meitrati  /,ur  Krkenntniss  der  Ih-i  Nephritis  auftreteiidcn 

Hypt'rtDp:  ie  des  liiiken  Heizeiis.  Virchow's  Arciiiv,  1S2,  p.  S27 . 

27.  Virchow's  Archiv.  80,  p.  29.">. 

28.  Consult  IVarce.  in  the  .Journal  of    Kxpcriinental  Mcdicint'.  x,    l'.K)9,  p. 

T.ih  ff. 


NOTKH    AND    HKKKHKNfKS 


2i:{ 


•21..  Meltz.r:  IxTturr.  ....  (K.i.n.u.  A....ria...  M.ai.i....  l!HI-».  12.  »,  .....I  :.. 
SturlmK:  I.-tuns.  U..c-.-t,  I'.Hm,  May  '.M-  M.  S-,- ..U:  Ada...., 
I'ri.nipU'H  of  I'litliolonv,  ii,  p.  !»•:*  'T. 

^.  i..,K,r,u...  i..'tiu. an.  ti ..rv...io..s  „....!.. ...  -.-;;";;; 

...phritis   i„.l.......l   with  ..hr.....i...n   u...l   ..m...u".  .Halts.        •"•:"" 

Jl  ,.ru,.iu...  l...tl.  pn,.l......  a  ....pLriti..  whi.-h.  h..w..v..r.  ...  t  ..   ...u.  r 

is  u..a......n.pa..U..l  l.y  ....l..."a.  wl.il..  th.'  latfr   ..  .«.s.,.-...  .-.l  «.tl.  .x- 

tonsiv..  ....l.....a.     ll..i..ok..,  ,..or....v..r.  ha.s  f.......l   that     h.;  s.t.....   .^ 

ani.,.als  ,...is.„....l  wit  I.  ..ra..i.....  has  th..  pr..iH.rty  ..(  P5<h>'"'"P '^''^  " 

in  .„h..r  a,.i,..als.     Si„.ilarly,  it  has n  sh..w..  l.y  K.u^t  "•"'  >  ''-^T 

th..t  tlu-  l.hH..l-s..r..... ..f  .|..l.....at.mH  ...phriti.'s  ..a.is...  ....Tcise.  l>».ph- 

;,;.w  i."  ani,..als.     S...  als..,   IVarc.-.  Ar.hiv..  ..f  hm-rnal  Mod.c.ne. 

iii,  I'.HMt,  p.  42._'. 

32.  Oi.' (liw..».t.spa.inu..K.     Kciii/in.  1^>*4. 

Xi.  Kn-hl.  1..C.  .it.,  p.  12;*,  with  further  lit.Tutur... 


APPKNDIX 

Cl.ASSIKIt  ATION    OK    NkI'IIKIIIS 

I.  .\i  iihnlis  .-///////(X.    Cliiinly  swelling,  infla!iim:iti)ry  (i'«lcm:i.  ami  serous 

(Mil  late. 

.V< /</////'.<  iirolifirit:    ( 'liaractcri/cil  particularly  liy  inflammatory  pro- 
litVraliiPii  of  parciii'liviiia  cells. 

II.  \i  jihnli^  iliiji  iiinilii-ii  (t  ixii'ldlirii:  Marked  de^feiieratioiis  and  necrosis 

ol  tixeil  cells,  and  cellular  exudate  into  glomeruli.  peri)jlonierular  and 
iiilerlul>ular  tissue.  Inflammatory  proliferation  of  epitlieliuin. 
(  ast  forniatioii.     Frequently  licmorrlianes  and  i)roliferation  (»f  fi.\ed 

ceil>. 

III.  \ii>liiilis  iliiji  iiiniliiit   it   j>n>ilit<-tii(i:    The    exudativ<'   features    in   the 

liack«rouiid.  The  de;r,.n,Tative  (particularly  fatty)  changes  pronii- 
neril ;  ca-t  formation:  proliferation  of  epithelium  ami  formation  of 
epitiielial  jiiant-cells;  gradual  <'ollap.se  and  loss  of  kidney  suh- 
stance,  appcarani-e  of  leukocytoid  and  til)rol)lastic  cells  in  the  in- 
terstitial tissue,  with  the  gradual  formation  of  matiu'c  fibrous  tissue, 
first  patchy,  then  more  ilitliise,  Ilemiyrrhaijes  occasionally  ))resent. 
(iradiial  thickcninnof  lilood-vi'ssels.  with  occasional  infarcts. 

IV.  .\i  iilirilis   i>n>(liii-lini:     Cradual,    first    patchy,    then    more   dilTuse,    in- 

tlannnatory  oliiiteration  of  renal  parenchyma,  leadiiitJ  to  general, 
particularly  cortical.  lo«is  of  kidney  suhstance.  Aliundant  over- 
jiniwth  of  fibrous  connective  tissue.  (Iradual  change  in  the  ty))e.s 
of  secretory  epilhehum.  Marked  thickening  of  hlood-ves.sels.  with 
eventual  narrowinj:  of  lumen  and  oliiiteration.  As  the  result  of 
these,  infarct  formation  with  healing  I'.v  ^'"ir  tissue. 

NilN-IM  l.\MMAlo[{V  F.KSIONS  oK  TMK   KinNKV.  ()(  (  ASH  )\  AI.I.V,  HI   r  \Vui)N(iLY. 

( iuui  I'Kn  AS  NKi'iiurns 

1.  Iii(liin:liii  fijiiiiiiUcii  riiiinii:  The  <'yaiiotic  induration  of  the  kidneys  re- 
sulting from  mitritive  disturlpanc<>s  as  the  result  of  ioiifi-continued 
venous  -tasis.  Connotioii  of  all  vascular  districts,  taking  origin 
and  remaining  markeil  particularly  in  the  medulla;   accentuation  of 


•-'It 


AIM'KNDIX 


21.') 


11. 


.,11  MKirkii.K>  I„11ow(m1  I.v  .riiciiKitoiis  ini!.il.iti..n  of  the  parts;  hwal- 
\,,.,\  atn.pl.v  an.l  .•..llu|.sr  nf  ki.ln.'V  suLstanc.'  witl.  .■•lually  U>vM 
fil.n.us  tissue  tjn.wtl..  Sr,-..n.la.y  .•luinti-'s  in  l.lc.a-pinincnt,  <ltH- 
t.,  |„.in.>lysis  aiKl  scttiiisi  Ire.'  <if  cimiips  of  i.lood-pitjmcnt. 
U,.„;,/„„  ,,/  srhrosis  rnnnn:  TW  srnil.^  atro|.l,y  an.l  sclerosis  of  tlu- 
ki.hwv  Sli-iit  an.l  imt.'hy,  to  ..xtrnnc  an.l  sicuMai  atrophy  aiul 
ohlit.-ration  .,f  r.M>al  pan.n.'hyn.a.  will.  n>ark..,l  artHioscU-rosis. 
..Miteration  of  vcss.is.  an.l  infar.tions.  Dilatation  oi  renal  pc'lvis 
with  n.ark...!  iMvakinj:  ui.  ..r  loss  of  its  .lastir  n.uscular  layer.  Hv- 
,,n..„llv  a.l.liti.M.al  stasis  with  <e.l..n,a.  It.  e.Ttain  eaM's  the  arteno- 
-,.l,.r..t'i.-ehan.^.'sinuch  less  proiniifiit.  infaiTti.M.s.  therelore.  luekinu, 
ami  tlw  ki.lniy  pivsents  a  simpl-  .liinh.ution  in  si/e.  with  r.'latively 
siiioiitli  s'lrfacr. 


W     :! 


L 


INDEX  TO  AUTHORS 


Adami,  r>7, 1J.J,  i7:i 

.l-'.tius,  4 

AUwcht,  .")7,  .IS,  l'2:i 

Altmunn,  52 

Arnold.  tM) 

Awlu.ff,  14,  ti4,  1J:{,  124,  ITS,  17',t 

Ashor,  :«• 

Aut  r<ht.  112 

Avi'onna,  5 


Cutunii",  ."> 
Councilman,  is,  107 
Cruikstiunk,  .'> 
Ciwhny,  ;<:«.  :«• 


Dblakiklu,  24 
Desir,  S 
Dnwr,  :j:{,  :{4 


Bam»k.iu;ek,  1st 

Hang,  ll'.> 

Hartrls,  Ki,  IS,  U)3.  17S,  105 

Baupr,  UtJ 

Bauni,  14S,  16S 

Baumuarten,  60,  100 

Book,  ISS 

Bocqiiorol,  0 

Boor,  14,  22,  t)0 

Benario,  .w 

Bonoko.  1-20 

Bortini,  2S 

BiorniiT.  is 

Biroh-llirsohfoUl,  .'>•') 

Bossard,  122 

Bowman,  10,  14,  20,  :U 

Boy.l,  ;« 

Brando,  ,"> 

Bright,  .1.  .■..  7,  10.  ltV2.  lo:{,  is:i,  1S.V  iss, 

io:i 
Brodio.  41 
BiiHk,  10,  11.  HV.2 
Biitsohli.  12:i 


KUKHOIILS,   l.")4 

Khrlioh,  ISO 
Elliot  son,  S 
Kngol,  i:« 
Km-st,  1(V2 
KwuUl.  170,  1S8 


Fahk,  ItHt,  170,  17."> 
Fisohlor,  117 
Krorichs.  7,  11,  lt>2 
Frio<loman.  170,  17:5 
l"rio<llaniU-r,  07,  Oil 


(lAI-KoTTI,  .')7 

tionost.  S 

Clugo,  0.  10 

Ciooth<-.  ^IHl 

liolgi,  00 

(ioodsir,  14 

Gottliob,  30,  40 

Ciravox,  S 

Grogory,  7 

Gull,  If.,  lt>:»,  170,  IHS 


Casstatt,  10 

ChriHtison,  7,  S,  l.i,  102,  lOiJ 

CV,hnhoim,14,  1.-.,  10,22,.V..  1.S.1S„._1M,. 

187.  liH),  101,  102,  104,  19,"),  I'.Hi,  10. 

Coplaml,  S 


Hai,i..  154 
Hiwonfold,  1S4 
Hausmann,  30 


217 


^!r 


21S 


1M)K\ 


llx'lll.  <l 

llciiickc,   l.'i.   Hi.   i:.  (111.  !l!i 

HimIc.  III.  -.'s.  :!ii.  liKi.  iiij.  Ill: 


II. 


■rniic. 


:!ii 


ll.TxIiciiiiii-.  i:;i.  1  17.  I  !>>.  \r,\ 

ilcllllllCl.    Ill 

llirvcli.  IM.  iss 
l|i>l'iii:iii.  III! 
Iliirn,  Hill 
llili'trr.  |:il 


.M.iivl, .111,1.  ■-Ml.  I."..  Hi.  17.  lit.  Hi:!.  1711.    17.". 

Miiriliiiiil.  i:il 

Mc'lizir.  I'.ll 

.M.y.r    Kriilii.  :«•.  to 

M.v.r  .Il;iii-i.  ;{:i,  :i'.i 

Milii.'.  i:u.  I  l>i 

Miii'uiii'iii.  ."i 

Miillii-.  Jii. -'1.  :!l.  11.  l."i.  17.  III.  l.'iO.  Hi:!. 

;si 
.Miiiik.  :i7 


't, 


\i 


l-IHKI.    IIIJ.    \\<\ 


.)\NKw  \\.  mil 

.liiliiixiii.  Id.  I  I.  Hi.  Ili'J 
.Ions,  Ki'.l.  1711 


l\  MVI  Nsll  IN.    I'll 

Kaiifniaii.  .">li 

Kicl.s.  I.-..  Is,  .-,•;.  (i7,  IIL' 

Klitziiiski,  I  IS 

Kldtz.  IJ-.' 

Kiinui.vi.  to 

Kraus.  I-.':! 

Kr.>hl,  isl,  ls7.  I'.lll.  I!ir. 


l.WDKHKH.    MMl 

l.aiiil>lriii(l'.  ."ili.  •■|7,  nil 

l.aiiiiliaiis.  Ili:> 

l.rl..'(lrlT.   llr, 

l.ryrlill.  7.   Hi 

I.i.li'liiiiii.  Isii.  HI."..  I'.Ki 

l.i.l.r.i.li.  IJI 

l.itl.'ti.  UK! 

l.<.lil.iii,  -Ml.  -'1.  1."..  1117.  111.  IJI.  i:::!.  Hi:i 

Liivvi.  :i!l 

l.iil.ar-.li.  111.  IIIJ 

l.ii.lwin.  :il.  :iJ.  :il.  :i."..  :!ii.  ■',''.  m.  II.  isii. 

I'.ll 
l.ii>k.  I  Hi,  117 
l.vi.ii.  '.i:!,  '.I'.i.  inj.  lo:i 


Mai, MS.  :!<»,  HMi 
Matiti.  Ill 


\  i:i.i  I  I.  .".7 

N,-.>M-.  Ill 

Nauwirik.  Is.  (il.  1.7,  17s 

\i. ■111:11.11.  Hi 


(llll.l.KK.  .')" 
Ill-ill.    is.  ."I'.l.    llll 

I  Ishiiriir.  7 
Oswal.l.  IJ.". 
<Iv.it, .11.  IIS 


I'VN/.KH.    IJI 

I'assl.T,  IS4 
I'.rls.  101 
i'ctl.'iikiifi  T,  1  Hi 
I'laiiii.il.r.  :i'.l 
l'(lii(£.T.  II  ■ 
r.inli.k,  i:il.  I.".l 
I'rvin.  Hill 


Uanx.n.  UI 

IJa.v.r.  s.  (I 

U.-iiilianlt.  7.  II.  I.'>,  Hi.  H>J 

IfililMTt,  I."..  Xi.  07.  '.i:i,  '.It.  llll,  lo:{ 

Hiii,||l,i-,li.  .".li.  170.  17:! 

|{,„kii:iii-k.v.  1  1 

H,iiiil..iii.  |s| 

li,,~,nl,l,l.  llll.  117.  UJ.  IJ.". 

|{..Ml.>lrill.   I."..   HI 

l{,,-,iillial.  UJ 

lii.tli.  170 

li,.M,la.  III.  llHi 

li.iv.  :17 

|{ui...».  IJt.   IJ.". 

Itilliipf.  iir. 


INDKX 


219 


Sahatikh,  '^ 
SilirrcT,  10 
SiliilliiiK.  •'"•' 
Silimails,  ItMl 
Schinidl.  l'^" 
Schiiioll,  122 
ScuiiaiiiDrr,  •"> 
Si'iiiitiir.  Iti,  In, 
is.j.  1S7,  ISS 

Si<'l»>l<l.  10 

Siiiicin.  10,  lt>'- 

."Nilmi,  '• 

Sl.irlinii,  I'M 

Strwiirl,  Iti,  Ki'l 

Sicvrcr,  i!'.' 

Siiiion,  If.,  ll>:i,  170,  Iss 


10.  JO,  ;i.'>,  ;!T,  o;i,  i,v>,  n>;!, 

IVI,  I'.Ml,  lO.'i,  l!Mi,  107 


Vm.kntin,  (I 

Villi  C'cill.  l-'il 

Villi  ill.ilT,  ;!:i 

Vtnvorii,  -'i^^ 

Vinhim,  11,  r.',  l:f.  It,  1.-.,  10,  \-.22.rvl, 

.->.->,  .V),  •■>!•.  00,  Ot,  <>•■>.  II.-.,  117,  UN,  V2.i, 

170 
V(.)£(l,   10,   IJ 
Villi   llilllSCIllilllll,    IJti 

vmi  Kiililili'ii,  ti4.  S.^i.  Mi 
villi  Kcckliniiliiiii^^i'ii,  ■'>'i 
vi.ii  \iiil,  1  Hi 


WAIiNKIi,    IS 
\Vri)£.Tl,  14,  17,  IN,  iO, 
KiJ,  17S.  170,  ISO.  ISl 

\V<issn«rl.<T,  101 

Wrils,  .-. 

Wiililiiiili,  i:u 

Wilks,  l(>,  ItiU 

Willis,  s 


>:i.  1.0.  04,  liv-',  l->i, 


Taisk.  1 
Tlirlrinunii-  l-'.l 
Tliiiniii.  ■>»>.  ">".  !""•  ''•" 
■niuilirJii  .1,  110 

'rifsoi ,  s  , 

Trf::'iri:^.'.s"  is.,  ,.>,  is7,  .oi.  .o.     Z.kuuk„,  is,  .o,  m,  i:«.  .0:1 


INDEX 


AriTK  intcnilitittt  nephritis,  vu-w«  on,  IH 
piinnchymiilous  ai-Rvncriilion,  4.i 
usi"  i)f  woril,  '2;t 
AlbriM'lit's  views  on  pnitoplusni,  .')" 
Albuminuria,  first  demonstration,  .') 
in  fatty  stage.  \-t~ 
in  productive  nri>hritis.  l^^i 
in  simple  nephritis,  ."ii» 
nephritie,  urinary  (juolient  in.  41 
orthostatie.  urinary  (luotieni  in,  41 
phy.siolofiie.  urinary  ciuotient  in.  M 
Solon's  views.  '.I  r       ii 

Alkalinity   of   plasma,  diminution  of,   l-», 

IJ.-)  , 

Altmami's  tiranules  in  par.iul.ymatous  d.- 

neneralion.  •"'- 
Amyloid  deposits.  i:U 
Anasarca.  VM.  l'" 
Arsenic,  adema  from,  1!M> 
Arteries  in  proiluelive  nephritis.  lliV,  !•>'.• 
\rteriocapillarv  fibrosis.  Itv?.  1*^*> 
Arteriosel.Tosis  in  pro.luctive  nephritis,  UW 

splanc'hnic.  Mood-pressure  an.l,  ISSs 
Arteriosclerotic  kidney.  174 
\*her's  theorv  of  urine  secretion,  -V.) 
Atherosclerosis  in  pro.luctive  nephritis.  Ul'J 
Atrophia,  '-•'' 
rciiuni.  1"4 

vel  sclerosis  rcinmi.  '.il'' 
Atrophv  of  nlomcruli.  i:!;i,  l.">l 
Autolysis,  (iranular  deceneration  and,  .>. 
Aulolytie  processes,  til,  !!><,  1-'^ 


Hkiitim.  <'olumns  of.  '2S 
Hil.lionraphy  of  fifth  lecture.  Jit 

of  tirsi  lecture   ■.'1)1 
of  fourth  lecture.  JOit 
<if  second  lecture,  211.) 
of  third  lecture.  '.'07 
litailder,  discharne  of  urine  into,  41! 


HUkhI  in  urine,  first  (U'monstration,  .'> 

water  in.  urine  secretion  anil,  :i- 
HliMMl-pressure,  ISH 

suprarenal  (rlands  and,  I'.l'i 

urine  secretion  and,  •!! 
»lo<Hl-supplv  of  kiilney.  -.'"i 
HloiHl-vessels.  .edema  from  injury  to,  l.Hi 
IViwnian's  capsule,  21' 

theory  of  urine  s<'eri'tion,  31 
Bright 's  disea.se,  li-sions  included,  3 

oh.servations,  tl,  7 
Busk's  viiws,  11 


("anstxit's  views.  10 
Capillaries  in  productive  nephritis.  173 
Capillarv  endothelium,  proliferation  of,  ><b 
Cap*"'!'"'   <<'nneetive-tissue,  (jloinerular   rc- 

plaicinent,  147 
Capsule,  Bowinan's,  '.Mt 

epithehum  of,  prohferation.  Sf. 
in  deuenerative  nephritis.  •■>■ 
in  exudative  nephritis,  6S 
in  simple  nephritis,  4S 
of  kidney,  epithelitim  of,  30 
Casts  in  i.roduetive  nephritis,  1S;1 
Catarriial  inflammation,  detinilion,  13 
Cellular  casts.  UK) 
Cerebrosides.  chemistry  of.  120 
C^'Srtalion  of  symptoms.  113 
Chara<'t eristics  of  inflammation,  i! 
Chemical  causes  of  (edi-ma,  19S 
theory  of  blood-pressure,  1S4 
Cholera,  kidney  in,  4.") 
Cholesterin.  IIS 

chemistry  of,  120 
Cholesterin-ester-fat  infiltration,  V2i 

Choliii,  Hit 
Chromatin  masses,  (14 
Chromium  p«)is.mini£,  kidney  m,   »■'' 
Chronic,  use  of  wonl,  '23 

221 


•>•)•) 


INDKX 


('l:i>-itir,iii.iii.  I.  :;.  I.  ji.  >;:,.  .'i  i 

(  liiiiily  >\M  lliiiu,  .'r.' 
"riiiiii.  .Vi 

('..lli>hi  ImuIk'-..  II  I 

('iiliirnii^  111  Uiriiiii.  J> 

CcplTiTlillir    i:ll'i||;li'     lix  |irrl  nipllV     III     IM 

nil-,  Is.'i 
('Mlllliili\i'-tl"llr  cli:iln;i-,    |H7 
ill  iMiiy  i|ir'tiii;iiiiiii,   |:!( 
('(iiilr:ii'li'<l  ki<liii'\     ir>l.  Hi'.' 

-rcm.l.irv,     111,     I  IJ.     |,"iJ,      ,<.(■ 
S,,;inil'ini  finlr.uhil  l:i:lin  ,/. 
CorniMM-  ,-iil>liiii:iir   |Mii>iinim'    kiilm  v 

1".,   Hi.  no 
CiirtiA  ill  ■lii;(iii-i:iii\i>  iii'|i|ii'ili~.  Us 
ill  r\iiii:iti\  f  iii'itlirili*.  (is 

ill  »illl|llc'  Mi'|illlili~,    Is 

.if  kiilnrv.  ■-•7 
CrcMTiil  piciiiri's.  s(i 

('rilll|«il|»   illl1:illllll:lllnll.   ■Iilillilinti.    1 1! 

('rviisrii|iy  iif  iiriiii'.  ■>■> 

( 'viiiiiiiir  iinliirMiiiiii  ill  iMplniii-,   I.Vt 

('ylin.lnii.l..  Ill:; 

("y-t-  III  pniiiiirnM'  Mi'pliriil>,  Itis 


Dkc  \r--i  I,  viiiiN,  l.")l 
I>i't;i'iii'i','iiiiiii,  L'niiiiiliir,  -VJ,  .Vi 

iiriuiii,  ,'i."i,  ."i7 

>ii;iiilir:iMri',  ,'i,'i,  ,')7 

p:iri'lirliyiii;itntl-,  lit 
:irllli',    l,'i 
in  "iiiiplc  iiipliiili-,  .">■_' 

!nii*rti--ciipir  ;lppr;ir,-|lli'i'*,  .'I'J 
without  llitl;ilnll);l1  lull,    l.") 
Di'lIc'iiiTulivr  i\ii  l:iti\c  iH'pliiili-.  li:! 
ri>>-:ili(iii  iif  >yiiiptiiiii'-.  II:! 
r:ilty  chaii!;!-.  1 1  1 

I'lllli'tidll.'ll  C'li;illl£l'S.    Ills 
Hill"  ;ippi:il;lllii<,  lis 
lii«liii;riic-i-.  li:; 

lllirlo-i-..pic  :tppi;ir:tlli-'-,   S."i 

iiiiiniiiiii:il  ili.iiinis.  1 1  ! 
iriJi'Ml.l   ill,    |S',I 
p'llllii(;rlii-i~,  (i:l 
pliMll|fti\r  rlhirini-   III.    I  HI 

pni|iiiii-i>.  1 10 

li'l:iti'.|  kiiliiry   ili:iiiur-,   I  ,"iS 

tv,,i|i~,    1  10 


pll- 


Drp'llrnitlVi'   i'\llilMli\i'  lli'plllili,^.  trrillill:f 

tiiiiix.  110 
uriiii'  ill.  Ills 
I  III  I  y  iicphrili-.  1 1.'> 
lV,iiiin>,   !•") 
II'  plii'iii-,  li:! 
i;iii-i«,  Ii7 

lifn-*  ,ippi',tr;lIli-|->,  tis 

hi*tni;('iii'-i",  ti:» 
piitlmm'tiois.  Ii;l 

l)i:llirti'-  ill-ipilllls.   lirilli-  iif.    111 

I  )i:iuiMi-i~,  c'.'irly.  1 12 

ill  Villnll>  »t;isi-,   I.V'i 
I  )i-Miiiiilii-iiiiiiiii-plici>pli,itiil( -,  iliiiiii>iiy  i)f, 

ll',i 
l)i>cnM>.  rliMiiuiiii:  cliiirarlrr  III'.  :! 

iiii'lilili'ii.  JI 
l)i-t(ar\l-liritliiii,  IJIl 
|)iiip,-iy,  kiiliii'y  clitiiiiic-i  .itiil.  ."),  1) 

livrr  rlialllli'-  :llli|.  li 
l)riiu~,  ui|i'iii:i  liiiiii.  l!Hi 


!■!(  iKMiiir    ciriiiiir    liypcrlidpliy    in    iicpli- 

lili>.  Is.', 
I'lii(l:irl(iiti>  liliiii^M  ill  priuiiii'iivi'  iK'pliritis, 

170 
rjliliilhrli.'il  I'i'lls.  I'li.'iliKrs  ill.   107 
I'liiiliitlii'liiliii.  i:ipill:iry.  prnlil'iT.'iliiiii  nf.  Mi 
li!il:ir^riiiriil  ol  kiiliiiy.  Il."i 
l'.pillii'li:il  ui:iiit-ri'll-  ill  ii<'plirili>.  liO 
l')pillirliiiiii  ill  f:i1ly  ilriii'iiiiatliiii,  H'.l 

ill  siiiipli'  iK'pliriti-.  .■>! 

Ill'  i-ap-iilc  III'  kiiliirv.  :{0 
priilircnliDii.  S(i 

III  uliillli'I'llli,  '.".I 

III'  limp-  of  Iji'lili',  :iO 

of  tlll)llll>.  •_".» 

rills  ,|rri\c  I  flMIll.  '.Ml 

iiiwly  foil I,  I  l'( 

proliferation.  !ll 

of  iiift.  prolifcr.iiioii  of,  S(i 
ICxlraniLiI  >vnipiiiiii~,  I'.MI 
l!\llil:ilr.  {•ollslitlli'Ill-  of.    107 

ill  sinipli'  niplirili-,  ."il 

oiiciii.  107 
l!\uil:ilivi'  Iratun-.   I."i 

nrpliritis.       .'si'i'      Ih  III  III  ml  in      i.rinliiliir 
iiilihrilis. 


INDKX 


22;i 


K*i'-i>ii"i'-.  I'lT 
l'';ilty  (l(iiiiiir:iliiiii.  II  t.  I  I"' 
ilisinliiiliiiii  I'f  fill-  l'-*> 
fiiiHtiiiiiiil  rli:iinji-.  I'lll.  I">''> 
llliiiiiiTilli  ill.  1-'' 
nlvioKill  iiillllllt  .Mill.   1  1" 
lillrllcil)lll;ir  \\yi-nv  ill.   1'>1 
of  liral-t.  I'.lt   IPiTil'lllMtC    1-1 
lulllllr~  ill.   I  1*> 
v:iMiil:ir  apiKiriilil-  in.  I''' 
iiilillrnlioii.  1  1  1.  II'' 
I'liiili-tcriii-i-iir.  \2i 
(li>iiiliiiti(iii  111'  ImI.  r.''i 
|'miilii>iiiil  ili:iiii:i'-.  I''".  '•''' 
tlomcnili  ill.  I'-'li 
({|\(  riiii-r>li'r.  I'-l 
intcrlolmlar  ti>>iii'  in.  I-''I 
mlmlfs  ill.  1  IS 
vjisculiir  ;ipii;il;ilii>  i".  I"''* 
iiict:iiiiiirpliii-^i>.  1-! 
Mi|)liiitis,  ili'Ki'iirnilivi-,  ll.'> 
ictciirnilion.  1 1" 
>iil>s(;ilin'>.  (Icmnii^lnili'iii  "I-   1-- 

iii  acKi'iK'nilivc  iMi.hilivr  iir^plirirH.  '.H. 

107 
irhtjin.  1 1'> 
-iliiiitii'Miiii'.  1 1.' 
IVvir  iliilir  ill  >imp'i'  n'plnili^.  "'■' 
l'il)nisi>.  :irtiTiiii:ipiU;iiv.  l"''-i.  1^"^ 
Kihroiis    tissiir    priilifcniiioii    :i"'l    p;ircn- 

iliyiii:ili>ii>  liiss.  KiJ.  ITS 
Kiflli  liMliirr.  nil 

l)il>li(iiinipliy  111'.  Jl  1 
rill  nil  i'lii  llii'ory  of  iiriiii'  ^icnlioii.  M 

(il)jiclioii~  lo,  :!l 
I'irsl  Irilurr,  1 

liil)lio)jr;ipliy.  -'Ill 
I'InicI  f-it.  ciimlsiticMiioii  of.  IJ:'. 
I'liniis  of  Hiiulil'^  <li^'':'^''.  ' 
I'oiirili  li'i-iurc.  1 1(1 

l.il)lio»£r;ipliy  nf.  -'O'l 
I'ri'cziim-poiiil  of  iiriiii',  '■^'■' 
Iri  riiliV  vir\v~.  II 

l.nclioii;il  llii-oiy  of  IhkIi  l.loo.i-pn'»iirc.  Iss 
|.|lii(tioiis    of    kiillicy.   imllioloniral     v:in:i- 
lions  anil.  -" 
vii'ws  on.  -7 


Cii  \M-<  i:i.i.>  in  iiiplirili^.  •><• 


( lloiinriili    -S 

iiltiralioii  ill  -'"'•  I  '"* 
..ITiTlsoii.  nil.  Ill 
(  pithi-lial  liniiii!  of,  ■_".» 
fiiriiialioi'.  Js 

ill  iji.urmr.iiivi'  nipliiii'>.  <''S.  s."i 
ill  fitly  ili'irmriiiiion.  I'Jii 
in  priKJiirlivr  nrplirili-.  HH'.  Hi" 
ill  <iinpli'  iicplnili*.   Is.  -il 
Cloniiriilo-iiipliliii'.  I".  -'■  '•'■'•  '•" 

proiliii-livc.  1 1'J 
(ilynrin  pliu-pliorir  ari.l  in  nnni'.  I-" 
Clycirin-olii-la'   inlil'ralioii.   l'J» 
( '.lyoiirn    roiilcnl.  fatly  .litfin'Tali-m  ami 

117 
(naiiular  (■a>l«,  HKI 
ili'lirniialioii.  .'ij.  '<'-\ 
origin.  •'>•''.  ''I 
r-inniliraiHi'.  ."i.").  •''" 


iMiilativr 


II  M  liMiiMi  piitiiii'^.  sr> 

ll.ail.  rally  ilrp'i.nalr.l.  fat  pm-rnlaur  Ml, 

I-' 

liypiiiiopliy  of.  ill  iic|)linii^.  ls« 

in  nrplirili-.  ls:i 
llciiliMiliainV  lliiiiiA  <if  iirin.Mirri  1(111,  -i' 
llcinatiiiia,  lir-t  ili'iiiiin>l laliiin.  •"' 
ll.nioirliau;"-     in     ilitfini'raliv 

iii'pliriti-.  s."i.  !i;! 
ll.iiiorrlianii-  ncplniti-.  l'>-> 
llciilc.  loop- of.  -'S 
cpitlirluiiii  of,  :V) 
virws.  Ill 
llippiirir    aiiil    froni  sLv''"'-"  ^•"''   '"■•"'"" 

acid  in  kiilniy.  •!•"> 
Ilistoloitiial  invrslinalion-.  '.» 
llisloloay  III  kiilni  y.  -~ 
llisloriral  riviiw.  1.  -I.  *1 
llvaliiiili'i'lii-    II' 
Va-.l>.  ItNl 

I'oiislitiili'in.  IIHl.  HH 
tliroiiilii.  ".I^i 

inin-forinalion.  i:i:i.  l^i^-  1  *" 
llvilrainia.  1'.'7 

llviliaaiii.'  pli'tlioia.  udiina  ami,  lll.^ 
llyilroiH'pliroMs  in  sniili-  kiiliu'V,  1T7 
Hy.lrops.  19:! 
irritations.  IIMI,  li>7 


224 


INDKX 


llvpcniniia.  ai  live,    iiitmiliii    imtiiIoii    hi, 

a; 

siMliiiiu  rliliiriil  rxiTrlicin  in.  -i'.  ^^ 
iiritir  sccrrliiiti  in,  '^7 
III  il((£ciiiT;ilivc  cxiiilalivc  iirplirilis.  HM 
ii'clciiia  :iii<l.  KU.  1!)'> 
llyprrriiiniii'iisatiiiii,  IMt 
lly|Mrtr<>|iliy.  r;niMs,  "Hi 
of   iiKils  (if  :irtirii>   in   |irciilii(;livr  iicpli- 

rilis,  I7:t 
of  Klniiirnili,  1  1^ 
(if  li(':irl  ill  iicplirilis,  1*>4 
(if  tiilmli-,  ITiO 


|\i 1  .Miniiii   iiijiitiimn  intii  ri'iml  iirlcry, 

wlicrc  fiiiiiiil  iifliT,  ;i."i,  M 
lniliir;iii(i  iy:iiioti(;i  rcnuin,  'Jl  t 
Infiircts.  ITii 

Inllaniiiiiitiiin.  (■li:ira(l(Ti.'<lirr<  (if,  :l 
ciiiici'plidii  (if,  it.  tia 
(li'tinitioii.  I'J 
InHiiinniaiiiry  pnicc^i^r^,  intcr?(tilial  ctiannrH 

in,  IMI 
Intcrldliar  artery,  'Js 
Iiitcrlolmlar  arteries,  ■J'^ 

tissue  ill  fatty  st;n£e,  1.11 
Iiilcnial  re-'i^taiii  (•   within  renal  ciiiMilatiiin. 

I'.ll 
Iiiterslitial     anil     paiinctiyniatMiiti     furiii.H. 
ilisciissiiin,  1  t 
eiinneetive  tissue.  1  1 
hyperplasias,  early  work.   I  1 
iieiihrilis.  ihronie.  ItH      See  also  I'nnl-ir- 
liii  III  jihrili^. 
primary.  H>:i 
views  on,  In 
tissue,  chaiujes  in.  IIU 
Use  of  leriii,  '2J 
iMieholesterin,   I'Jl 


KM-HiisrKltlN.    I'Jl 

Kephalin,  ll<) 

Kidney,  imatoinical  changes.  - 

anatomy  of.  -"^ 

arteriosrlerotie.  171 
as  lilter,  ;{1 

liliMid-siipply  of.  -*» 

capsule  of,  epithelium  of,  :iO 


Kidney    clialldes,  H 
colli ra('te(l,  Hil,  D'l'J 
cyanotic.  IVI 
red,  H>:t 

.s, iidary.  Ill,  II-'.  ••'•■J 

pnHliictive  neplirilin  and,   rchilions, 
1(V2 
cortex  (if,  'J7 

disease,  ditiiculties  of  sllldyuiK,  I 
historical  review,   1 
incliiiled  under  Urinht's  diseiinc,  Jl 
structural  and  functional  cliaiidcx,  re- 
lationship, 2 
enlargement  of,  1  M 
functions  of,  - 

patholoBi'al  variations  and,  27 
vii     -  on,  27 
(llotii     'ili  "f,  2S 

eiHthelial  linitiK  of,  2!l 
foriiialioii,  2'> 
hippiiric  acid  formation  in,  :<•'> 
histological  chann'i',  2 
liiHtoloKy,  27 
ill  cholera,  4."i 
ill  chroniiuiii  poisintiiiK.  ■♦■"> 
in  corrosive  sulilinmte  poisoiiinu,  •!.">,    Ul, 

m 

in  phosphiirus-poisoniiiK,  4."i,  lit) 

in  simple  iiephriliH,  47,  4S 

inner  part,  27 

larise  white,  1  l.'i,  M^ 

lymphalics  of.  2i> 

inedulla  of,  27 

extirpation  of,  urine  secretion  after,  ,'iO 
medullary  ray.s  of,  'Ifi 
nerves  of,  2!t 
outer  part,  27 

liatholottic,  dilTerent  from  normal,  44 
pelviw  of,  diMchar(£e  of  urine  from   \'.i 

in  senile  kidney,  177 

structure,  4i< 
productive  chaimes  in,  110 
pyramiils  of,  2S 
senile,  174 
struct  lire,  27 

synthetic  processes  in,  :<"> 
lutiercles  in.  formation,  tKl 
tubules  of,  2H 

epithelial  liniiiK  "f.  '-^<  •"' 

l.udwijs's  theory  of  function  of,  '.Vi,  3S 


INDEX 


225 


Kidnoy,  iirinury  clirDiMOKi'iit  i".  :*•'» 
vnMi'iiltir   iipimrnliis   "f,    in  f"lty    "'nH''. 
\Xi 

Koniiiyi'fi  tlicury  n{  uriiir  Mccrt'lioii,  »•' 
iiriimry  (|iioli(iil,  H> 

I.AioiK  wliilc  kidney,  ll.'i,  l.VI 
I^..illiin,  US,  11(1 
l,i|Mmls  US,  ll'.t 
l,i>lil('in'~  vicwM,  '.tl 

l,<X)|)r<  1)1    llt'Illf.  -S 

I'pitlii'liiini  of,  M) 
I.iiilwiK's  tlicory  of  fiuMiion  of  tulmlfw.  :VJ, 
Xi. 

of  urine  secrdioii,  ill,  M 
l.ynililiiinKitisin  nrplirili!*,  107,  I'.M 
Kynipliiitii-  clmnKef,  n'<l<'nm  imil.  l!Ki,   l!t7 
l.ynipliiiticK  of  kidney.  21t 

Mf.diANKAi.  causes  of  cardiue  hyiH'rtrophy, 

ISti 
MiMlidlii,  -27 

extirpation  of.  nrine  weretion  after,  ;W 

in  ileueneralive  exnilativi-  nephritis,  tiS 

in  simple  nephritis.  4!S 
.MeiliiUary  rays  of  kidney,  2H 
MeninRes  in  nephritis,  1!>:J 
Meyer's  views  on  urine  secretion,  W 
Mono-ainidi»-ili-ph<>«phatides,  chemistry  of, 

1  lit 
Mono-ami(lo-mono-p'""'P''"'''''''''      '••»■""»- 

try  of,  lilt 
Muller's  views,  2(1 
MiinK    iiid  Senator's  theory  of  urine  doore- 

tion,  H7 
Myehns,  US,  U'.t 


Nki'HKITIS  depenerativa,  'i'> 
adiposa,  -'> 
et  exililaliva.  !>:< 
exudativa,  -'i 
ha'tnorrhaitiea.  2."> 
prolifi-ra,  2it,  .V»,  til 
tin-  mphrilix. 
et   prodiictiva,   .">'.),  til.     See  also  I'ro- 
lifemtiiv  luiihritix. 
simplex,  24 
lU 


Nephropatliia  chronica  inflammiitoria.,  170 

Nephroses,  J.'i 

Nerves  of  kidney,  20 

Nitrogen  excretion  in  hyperu'mia,  :{' 

in  stasis,  117 
Non-inflammatory  proceiwes,  i 

wroiiKl.v  uroiiped  a.s  nephritis,  21 1 
Nutritional  channi's,  114 


(I'.liKMA,  Itil,  IKl,  1S1»,  HCi 

in  (h-Kcnerative  extlilative  nephritis,  KM, 
is'.t 

irritation,  l'.t7 
Oleyl-li'cithin,  120 
(trth's  views,  IS 
()smoti<'  prensiire  of  urine,  Xi 


See  also  I'rnlifera- 


I'Al.MITVI.-l.KriTllIN,  120 

I'aramyelin,  chetnislry  of,  11!) 
rarenehymutoiis  and  interstitial  forms,  (li>t- 
ciission,  14 
deKcneration,  <>4 
acute,  4."i 

in  simple  nephritis,  .")2 
micn)Scopic  appearance»i,  r>2 
inHammation,  definition,  1^ 

Virchow's  views,  12 
nephritis,  (edema  in,  1S9 
u.se  of  term,  22 
ratholottical  processes,  channinK  character 

of,  :{ 
I'elvis  of  kiilney,  discharRe  of  urine  from, 
4:{ 
in  senile  kiilney,  177 
structure,  4;{ 
Peric;>rdiuin  in  nephritis,  \SV.i 
l'eril..-mphaiiKitis  in  nephritis,  107,  194 
reritoneuni  in  nephritis,  19:5 
I'fister.  101 

I'hosphatides.  ehemi.stry  of,  U9 
l>hospl»)ric  acid,  ijlyccrin,  in  urine,  120 
rhosphonis-|M)isoninK,  kidney  in,  45,  116 
Phrenosin,  121 

l'hyto.sterin,  chemistry  of,  120 
l'la.sina,  alkalinity  of,  diminished,  124,  12.-> 
Pleura  in  nephritis,  191$ 
Productive  cliandps  in  kidney,  UO 
nephritis,  2.5,  Itil 


22(> 


INDKX 


rriHlii.iivr  ll(■|l|lnll^.  :ill>iiiiiiimii:i  in,  IV! 
artrriri"  III.   ll>7.   HiM 
iiriirin^c  lrrip»i-  in.  H'>'',  IT  I 
Mtlii  ni-ilirii'-i-  111.  It'i'.t 
i;i|iill:irM-  in.  \~i 
( iinliiir  li.\|MTUii|iliv  ill.  I VI 
lu^ls  III.  Wt 
r:iu«r«.  I*i''» 

rirciilatiiiii  111.  Ii>7.  Iii'.t 
ry«l.-  ill.  Il'''» 

ciiilirtiTiii^  tilirii-:!  I'l.  170 
hliroii-  li>-iii'  prclifirtimii  in.  liiJ.  17>> 
|iiiiilic.n:il  ili;ini£r-.  Iti7.  I>«1 
llliiiiirrilli  III,  \*'*':  l'''7 
l[rll^^•  :i|i|M';ir;ilii>>,  Mil 
liviMrlriipliv  cif  rii:il>  nf  arlrrii  >  m.  17:! 
nilcnixcipir  ;llipi;ir;lllir>.  I''>"> 
piirriiclivliKitipii- lll•'^  ill.  !•>■-'.  17N 


.Si  Mii.vriN  VI  nrpliriii-.  \'.»< 
.SiliTll^H.   171 
riiiiiin.  -'< 
.Si  unci  Irrliiri'.  ■J7 

liililixitrapliy  <>l.  .'H.'i 
Si-niliiliirv  niiilriHii'il  kii|l"\.  III.  II.'.  I.VJ 
:iliatiiiiiii':il  rviilrnn-.  JI 
priHliiitivi'  iii)iliriii»  ;iimI.  ril:iii'iii-. 
Hi  J 
Srrrctlim  iii»l».  I'll 
.Siiiiliir's  vicwi.  \'.> 

llirury  iif  cariliin   li>  |..    in.pliy.  IVI 
S.'imliir   :iiiil  Muiik'-  lli.nrv    of  iiriiii'  -.cr. - 

Hull.  :I7 
.Snilr  kiilnry.  171 
pi'lvi>  in.  177 

Srrnll-  nirlnlirillicj'  III  111  |illflll>.  I'.''t 
Siriliii-:ill(iiiniii  in  iirinr.     -mt  MliHmiiiiinn 


.nnii.l.iry  rMiilr:.rlr.l   ki.lii.y   Mii.l.   H-       Siinpl.' ii.lilirili-..  »•">.  4 


l;ltillll>.    III-.' 
llllllllr«  ill.    Itili 
Ul'ilir  in.  I'^l 

viiMiil:ir  ili;iiii:i  -.  I'i7.  Hill 
l'riii£iiii>i-.  1 1" 

rri«lifiT:itiiin  ill  I'atly  ili«i'ii.r;iti(iii.  I  IM 
iif  (•piihcliiiin,  Mi 
(ll  lllllllliv.  l»l 

rnilifrniiivc  ii.plinii>.  -•">.  '>'■>.  •'>! 

fiincticinal  cliiiiiKi-,  '>:> 

urine  ill.  ti:! 
I'n.laBMii.  11^.  U".  I-I 
I'mluphiMii,  viiws  (111.  ."i7 
l•ykllll.-i^.  '.tl 
I'vraiiii.l-ol'  kiilmy.  Jn 


Uavk.h's  vicwf.  '.I 

Kcnivcry.  IHI,  111 

Ui'cl  kiiliiiy,  Miiall,  Hi! 

Krilrx  llictiry  of  rarili:i>'  liyprrtnip'iy,  IsT 

Ucuciicraliiiii,  fatty.  117 

Ui'inliart  >  view.-.    II 

Ki^nal  arlcry.  .'s 

iiijntions  (if  iiiiligci  c  ariiiiii  iiilu,  whin' 
fciiind  after.  :t.'i.  :f(> 
.liarrliea.  :«• 
^^ylllptl.lll:<.   \W 
liepair  ill  inllainiiiatory  priiees>ef.'ls<» 
Hdckitaiiskv's  view^.,  11 


alhiiininiiria  in,  .'>!> 

epitlieliiiin  in,  ,'>l 

eMiilate  ill,  .'ll 

fever  urine  in,  ,'>1» 

fillietiiinal  ellallKe^,  *■'> 

([Icinienili  in,  1^,  '>\ 

MiiiTiweiipic     up|M'araliee«     "f     kiilney, 

:,\ 

pareneliymatiiii.*  ili'Heneralimi  in.  -VJ 
pallmliiuie  tii^tiiloitv.  17.  J>> 
ti'riiiinatiiiii.  -"iS 
lisKlle  liitwei'll  tllliule^  in.  ."iS 
nilmles  ill,  .VJ 
urine  in,  .Ml 
."icMlium   eliliiriil  ami   water   resorptiun,   :iJ, 
:«• 
I'Xi-retioii  in  liyiieriiiiiia.  :t7.  :tS 
uileiiia  ami.  1!I7 
Solon's  views,  11 
.Sphyiinoiiiyelin,  clieinislry  ■  i.  l  I'.i 

Splanelinie    arterioselerosis.    M l-pressuri- 

and. IHS 
Stanesofilisea.se,  Uri(!ht's  views,  li,  7 
SlainiiiH  aflinitiesof  tiilie-ia.sts,  lO'i 
.Sta.sis.  nitroijeii  exiretion  in.  :17 

urine  .secretion  in,  ;{7 
Siilpliiiti'  iiijei-tions  into  Mood,   urine  after, 

M 
Suprarenal  «lan.ls,  l)loi>d-pres.sure  and,  11>'J 
.Syinptoins.  I!t1* 
.•^yiillietie  pr<Mes.ses  in  kidney,  :i,') 


INDKX 


227 


'I'liiMi'  111  luri'.  I.'i 

l.ililhiliriiiiln  "I.  -''•" 
'riiriiinlii,  li.v:ili"i     't.l 

■|l«.,|r  l..)ttl'l(l  !llt>lllf».  .  |mll«l-  II'     I'M 

ni  f:ill\   -laK"'.  I'll 
!i  «imt>li-  tit|ilirlli-,  .'iS 
Tom,    'lic<ir\  I'l   liiuli  tiliKHl-pri^^iiri'.  I>» 
TnynlMT-  Mrtt-,   1 1 

Trni-uiliili'  •lyX".  I"l 

uw  i>f  Irriii.  I!'" 
■rriiiii"!!'   iiii'i'-"*'"'"'""'^   tliiiirv  of  mini' >>"•- 

IT'lil'll.     '"^ 

'I  ii-.iiiiiilii-|«li'"'lili!i'i'i'     I'" 
Trniilini'  iiiliiiiM  liiiiiK.    i".  ">^.  '-•' 
liilir-iii^l-    KKI 
r<'lliil:ii.   UN) 

111||1|H1-1I111I1.    1"" 

(traiiular.  Km 
tiviiliiii'.  M"' 

I'linslitiiliiiii,  MNI,  I'll 
scirotiuii.  Il>l 
"tiiiiiiiilt  iitliiiitir!".  UC- 
transuiliili     I'll 
waxy,  m) 

r<ili>litiltii>n.  HI*!.  1"'- 
TiilM-rrlcs  in  kiiltu'V,  fiirniiilioii.  tut 
Tiilml"  >.  -!>*. 

ililatatioii  iif.  HI' 
(■tTr(l>  nil,  111 
(•iiliirncmt'iit  of,  \M 
rl.illii-liiim.if.  St,  :«1 
nils  iliTivi-(l  from.  <•>.• 
newly  f(iriin-<l,  14!> 
pnilifcration,  !M 
in  ilfgrnrralivr  cxuilativi-  ncplirilis.  >X\ 
in  fatly  ili'Hi'nrralion.  14s 
inpnHitictivciiciilirilis,  UMi 
in  simplo  iicphrili.'*,  .VJ 
l.iKlwiu".-'  ilii'ory  of  funiiion  of,  :!-',  :t:{ 
'I'lifl.  apiM-arancfs  of.  Ml 


I  rinr  •  xannnatii.ii.  rarly.  I 
fiMT,  in  -iiiipli'  niplini)-,  .V.» 
fni/inii-pi'iiil  >'f.  -t'l 
uly.rrih  pdo^pliorir  anil  m    l',ill 
in  ili'urncraliM'  ixu.laliM    n.phriii-     KIH 
in  f.i'lv  -laili-    IVi 
in  iirixImliM'  mpliri'i".  1^1 
in  prolifiraiiM'  mpliritif.,  •■>;( 
in  -iinpii-  iiiplinli!',  'I't 
III  villous  -ta«i»,  I'i'i.  I"'» 
iif  ihaliili"  iii-ipiil'i-.  !'• 
ii.MlotIr  |»rrn»liri-  ol,  -l-l 

^IMTI'IlMll.    •" 

afirr  ixiirpation  of  iiiiiinlla,  :i'.i 

afliT   iiijcrlioii-    iiilo    IiIoimI  of  siMliiiin 

-iilphali'.  •!"• 
Xsliir's  theory,  -i'* 
liliHMl-prissiire  ami,  M 
Hownian'.-i  theory,  M 
filter  theory,  :U 
lleiileliliain's  theory.  :!."> 
in  hypera'inia,  ■!" 
in  .stasis,  it" 
Koninyi'.s  theory,  40 
laiilwiuV  theory,  M,  'H 
Meyer's  views,  40 
Senator  ami  Miink's  ihi-ory,  HT 
suininary  of  views,  II 
Iriiimuihition-seiTelory  llii-ory,  :i.H 
views  on,  it! 
water  in  lilooil  ami.  :V_' 


V.\!<  efferells.  Jit 

Va.seiilar  apparatus  in  fatly  staiie,  I.IH 

in  priHluitive  nephritis,  lt>7,  ItlH 
Venous  stasis,  1,')4,  11»7 
Virehow  on  paretiehyinatous  iiiftammation, 

\2 
Viseeral  changes,  llil,  ISil 


Watkh  anil  soiliiini  ehloriil  resorption,  :VJ, 
:«i 


luKTKH,  iliseharije  of  urine  into,  4:i 

St  met  lire  of,  4:5 

Iriniirv  ehmmoftcns,  formation  in  kiilney,          "■';'"''""'"•/-,„,  .,., 

by  tubules.  .12, -t-t 

'  '.■     .    ,,\  Waxv  ca-sts.  UK) 

niiotient.  40  ■                         ,  ,,,    ,,^, 

Irinr,  rrvoseopy  of,  lU  .  constitution,  1(X),  UYI 

.liseharge  from  l«.lvis,  Vi  ^^  '-'K'-f'  ><  ^"•"■^'  ' ' 


